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Cancer Care Block > Haematological Malignancies > Flashcards

Haematological Malignancies Flashcards

1
Q

Where can haematological malignancies arise from?

A

Bone marrow
Thymus
Peripheral lymphoid system

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2
Q

What is an acute haematological malignancy?

A

Those that appear and progress over a short time scale (days/weeks)

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3
Q

What kinds of cells are usually present in an acute haematological malignancy?

A

Morphologically immature cells (blasts)

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4
Q

When should an acute malignancy be treated?

A

Immediately!

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5
Q

What is the time scale for chronic haematological malignancies?

A

After they appear they may stay stationary or progress over a longer timescale (months-years).

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6
Q

What do chronic haematological malignancy cells look like?

A

More difficult to distinguish from normal cells morphologically

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7
Q

What are the 2 main types of acute leukaemia?

A

Acute myeloid leukaemia and acute lymphoblastic leukaemia

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8
Q

Are there other types of acute leukaemia?

A

Mixed or undifferentiated

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9
Q

What is the incidence of ALL and AML in the UK?

A

Approx 1000 new cases of each per year

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10
Q

Who does AML affect?

A

People of all ages

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11
Q

Who does ALL affect?

A

Most common malignancy in childhood, but does affect adults also

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12
Q

What happens in ALL?

A

Proliferation of lymphoid blasts (B or T cells)

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13
Q

What symptoms do pts with ALL present with?

A

Symptoms of pancytopenia

Bone pain

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14
Q

What are the symptoms of pancytopenia?

A

Tiredness/fatigue/breathlessness (anaemia)
Abnormal bruising/bleeding (thrombocytopenia)
Infections (Leukopenia)

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15
Q

What features may be seen on examination of a patient with acute lymphoid leukaemia?

A

Lymphadenopathy

Hepatosplenomegaly

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16
Q

What symptoms do pts with AML present with?

A

Symptoms of pancytopenia

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17
Q

What is the first phase of therapy for acute leukaemia?

A

Inducing remission by aiming to reduce or eradicate leukaemic cells from the bone marrow

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18
Q

Define remission from acute leukaemia.

A

Normal FBC and less than 5% blasts in the bone marrow.

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19
Q

How many AML pts under 60 achieve remission?

A

80%

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20
Q

Aside from chemo, what can we potentially do for acute leukaemia?

A

Allogenic stem cell transplant (depending on risk group)

Palliative or supportive care, depending on pt needs

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21
Q

How many children with ALL are cured?

A

80%

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22
Q

What are the characteristics of chronic myeloid leukaemia?

A

Chronic myeloproliferation -> increase in neutrophils and their precursors, with increased cellularity of the marrow

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23
Q

What genetic change is associated with CML?

A

t(9;22) -> BCR-ABL gene

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24
Q

What is the 22nd chromosome also known as?

A

The Philidelphia chromosome

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25
Q

What is the aetiology of CML?

A

Unknown haha lol

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26
Q

Who does CML affect?

A

People of all ages with a peak between ages 24-45

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27
Q

When do CML pts usually present?

A

In the chronic phase

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28
Q

What are the most common presenting symptoms of CML?

A 
Weight loss
Night sweats
Itching
Gout
Left hypochondral pain
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29
Q

What are the rarer symptoms of CML, and what causes them?

A

Visual disturbance
Priapism
Headaches

Caused by hyperviscosity

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30
Q

On examination of a CML pt, what will you find and in how many pts?

A

Splenomegaly in 90%

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31
Q

What are the lab findings associated with CML?

A 
Neutrophilia
Prominent basophils
Abnormal platelets
May be anaemic
Raised uric acid
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32
Q

What can CML turn into and why is that bad?

A

Acute leukaemia, and because it can cause death

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33
Q

How can we predict outcome of CML?

A

Stage based on age, spleen size, blood blast cell and platelet count

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34
Q

What symptoms of CLL develop as the disease progresses?

A

Fatigue and SoB
Lymphadenopathy
Enlarged liver and spleen
Infection

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35
Q

How do we treat CML in the chronic phase?

A

Imatinib or other tyrosine kinase inhibitors

Allogenic stem cell transplantation

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36
Q

What can we do to treat the high uric acid associated with CML?

A

Allopurinol

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37
Q

What is essential thrombocythemia?

A

Chronic proliferation of platelets

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38
Q

How does essential thrombocythemia present?

A

Arterial/venous thrombosis

Splenomegaly

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39
Q

What can essential thromocythemia turn into?

A

Myelofibrosis

Can have leukaemic transformation over 2 years

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40
Q

What is polythaemia rubra vera?

A

Uncontrolled production of red cells (despite erythropoietin production being switched off), alongside other cell type production increases

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41
Q

What is lymphoma?

A

Cancer of the B and T cells i.e. clonal proliferation of lymphoid cells

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42
Q

What are the 2 main types of lymphoma?

A

Hodgkin and Non-Hodgkin

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43
Q

What are the 2 types of Non-hodgkin lymphoma?

A

High grade and low grade

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44
Q

What is low grade lymphoma like?

A

Generally viewed as incurable but not an immediate threat to life

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45
Q

What is high grade lymphoma like?

A

Immediate threat to life so need urgent chemo, but it has a good cure rate (~70%)

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46
Q

Which areas are affected in lymphoma?

A

Lymph nodes

Spleen, bone marrow, and some other areas can be involved

47
Q

How can lymphoma be classified?

A 
Descriptive
Immunophenotype
Cytogenic markers
Morphology
Site/cause of disease
48
Q

How can lymphoma present?

A

In many different ways

Generalised enlargement of lymph nodes, weight loss, fevers, night sweats, and local masses causing symptoms

49
Q

How is lymphoma diagnosed?

A

Histological examination of a biopsy specimen

50
Q

What is the incidence of lymphoma?

A

Increases with age, and increasing in general

51
Q

What is Hodgkin lymphoma?

A

Lymphoma characterised by presence of Reed-Sternberg cells (multinucleated giant cells)

52
Q

What is the M:F in Hodgkin lymphoma?

A

2:1

53
Q

WRT HL and lymphocytes, what type has the better prognosis?

A

Lymphocyte rich HL

54
Q

How is HL treated?

A

Depends on stage and symptoms.

Radiotherapy for early stage, and bulky localised/resistant disease.
Combination chemo for more progressed disease.

55
Q

Who does Non-Hodgkin lymphoma affect?

A

Pts of all ages

56
Q

What is the aetiology of Non-Hodgkin lymphoma?

A 
Environmental:
-EBV causing Burkitt lymphoma
-H. pylori causing gastric lymphoma
Auto-immune disease
Immune suppression
57
Q

What are the other causes of neutrophilia?

A
  • Infection
  • Inflammation
  • Drugs e.g. steroids, adrenaline, toxins, GCSF
  • Myeloproliferation e.g. CML, PRV, Myelofibrosis
  • Solid tumours
  • Cigarette smoking
  • Bleeding
58
Q

What are the other causes of neutropenia?

A
  • Infection (viral)
  • Drugs (anticonvulsants, antithyroid, chemo, abx)
  • Immune mediated
  • Bone marrow failure
59
Q

What are the causes of lymphocytosis?

A
  • Infection (EBV, CMV, hepatitis, varicella)
  • Leukaemia/lymphoma
  • Stress (MI, sickle cell crisis)
  • Trauma and exercise
  • RA
  • Adrenaline
  • Splenectomy
60
Q

What are the malignant causes of lymphopenia?

A

Hodgkin’s disease
NHL
Aplastic anaemia
Myelodysplastic syndrome

Also chemotherapy

61
Q

What is myeloma?

A

Malignant tumour of bone marrow characterised by proliferation of plasma cells causing bone destruction and bone marrow failure.

62
Q

How are myelomas subclassified?

A

According to the type of antibody produced.

63
Q

Which subtype of myeloma is most common?

A

IgG meloma

64
Q

What is the preceding condition to myeloma?

A

MGUS - monoclonal gammopathy of undetermined significance.

65
Q

What is the pathophsiology of myeloma?

A

Plasma cell proliferation leading to neoplastic transformation of plasma cells which accumulate within the bone marrow and produce a monoclonal protein that causes organ and tissue impairment.

66
Q

What process causes osteolysis and hypercalcaemia in myeloma?

A

Imbalanced bone remodelling due to increased osteoclast and reduced osteoblast activity.

67
Q

How does myeloma cause renal impairment?

A

Malignant plasma cells produce excess monoclonal free light chains which are excreted via the kidneys, causing AKI and tubulo-interstitial inflammation.

There may also be dehydration, amyloid deposition, hypercalcaemia, and use of nephrotoxic drugs.

68
Q

How common in myeloma?

A

2nd most common haem cancer - incidence is 4.5-6 in 100,000 in Europe.

69
Q

Tell me about the demographics of myeloma.

A

Median age at presentation is 70.
More common in Afro-Caribbeans than caucasians.
M>F

70
Q

What are the most common ways in which myeloma presents?

A

Bone pain, especially backache.
Pathological fractures.
Symptoms of hypercalcaemia such as drowsiness, dehydration, constipation, nausea)

71
Q

What are some less common (but still important) ways in which myeloma might present?

A
  • Spinal cord compression
  • Lethargy (anaemia)
  • Anorexia
  • Dehydration
  • Recurrent infections
  • Syptoms of hyperviscosity (hearing loss, vertigo, headaches, seizures)
  • Bleeding/bruising
72
Q

What is a myeloma screen?

A

Basic Ix to be done to screen for myeloma:

FBC (anaemia, leukopenia, thrombocytopenia)
U&Es + Creatinine (impaired renal function)
LFTs (albumin, uric acid)
ESR
Calcium and bone profile
Ig levels

Urine protein electrophoresis

Plain X-ray of problem bone areas.

73
Q

What acronym can we use to remember what goes wrong in myeloma?

A

CRABBI

Calcium ↑
Renal impairment
Anaemia
Bleeding
Bone lesions/pain
Infection
74
Q

What are the monoclonal antibodies in the urine called in myeloma?

A

Bence Jones proteins

75
Q

What Ix can confirm a diagnosis of myeloma?

A

Bone marrow aspiration and trephine biopsy -> significantly raised plasma cells.

76
Q

How can we survery for bone lesions in myeloma?

A

Whole body MRI (CT is not suitable)

77
Q

Which 3 criteria are needed for a diagnosis of myeloma instead of MGUS?

A
  • Over 10% monoclonal plasma cells in marrow
  • Monoclonal protein in serum or urine
  • Evidence of myeloma-related organ or tissue impairment (CRABBI)
78
Q

Which Ix is used in myeloma to predict prognosis and perform staging?

A

Beta-2 microglobulin levels

79
Q

How should myeloma be managed, generally speaking?

A
  • Control disease
  • Prolong survival
  • Maximise QoL
  • Emotional and psycholoigcal support
80
Q

How can myeloma be managed in fit/young patients?

A

Induction followed by high-dose therapy with stem cell transplantation.

81
Q

How can myeloma be managed in elderly pts/pts over 70?

A

either bortezomib, melphalan and prednisone, or lenalidomide plus low-dose dexamethasone

82
Q

What maintenance therapy is recommended for younger pts with myeloma?

A

Lenalidomide monotherapy if they have undergone autologous stem cell transplantation.

83
Q

How should pts who are in remission with myeloma be managed?

A

Monitored at least every 3 months to assess:

  • Symptoms
  • Blood tests
  • Bone imaging where appropriate
84
Q

If myeloma relapses, what does treatment depend on?

A 
Performance status
Comorbidities
Type
Efficacy and toleration of previous therapies
Interval since last therapy
85
Q

How do we prevent/manage the complications of myeloma?

A

-Bone disease - zoledronic acid/other bisphosphonates
-Consider stabilisation of bone #s or bones at risk.
-Radiotherapy for bone
pain.
-Palliation as appropriate
-Infuenza vaccine, IVIg as appropriate
-Test for long term infections (Hep B/C/HIV) before starting Rx

86
Q

What is the prognosis for myeloma?

A

Better than it used to be, but still very variable.

Worse if present as an emergency or older pt.

Survival can be up to 10 years depending on individual.

87
Q

What can we use thalidomide for in myeloma?

A

Reducing paraprotein levels vie anti-angiogenesis

88
Q

How does polycythaemia vera present?

A

Fatigue, pruritus and symptomatic splenomegaly, along with an increased risk of thrombosis

89
Q

In polycythaemia vera, when is the pruritis worst?

A

After a hot shower or bath

90
Q

How does polycythaemia look on examination?

A
  • Plethoric
  • Ruddy complexion
  • Splenomegaly
  • HTN
91
Q

How is polycythaemia vera diagnosed?

A

2 major + 1 minor, or 1st major + 2 minor criteria:

Major:

  • HB over 185/165
  • Presence of JAK2 617 F mutation or similar

Minor:

  • Hypercellularity on bone marrow biopsy
  • Serum erythropoietin below normal
  • Endogenous erythroid colony formation in vitro
92
Q

What are the differentials for polycythaemia vera wrt raised Hb?

A
  • Volume depletion (dehydration, severe buns etc.)
  • Primary polycythaemia (genetic)
  • Polycythaemia secondary to chronic hypoxia, kidney disease, or paraneoplastic (erythropoietin producing tumours)
93
Q

What do initial blood tests look like with polycythaemia vera?

A

FBC - elevated Hb, paced cell volume, WBC and platelets raised too.
Ferritin low due to increased demand for iron.

94
Q

What does polcythaemia vera look like on abood film?

A

Plethroic phase - normal RBCs, varing degress of maturity in other cell lines

Spent phase - tear-drop cells, leukocytosis, thrombocytosis.

95
Q

How is polycythaemia vera managed?

A
  • Control cardiovascular risk with low-dose aspirin.
  • Cytoreductive Rx if high risk
  • Venesection to keep haematocrit below 0.45
96
Q

What is polycythaemia vera at risk of transforming into?

A

Myelofibrosis (10%)

Acute myeloid leukaemia (5%)

97
Q

What can we use to treat advanced polycythaemia vera, and how does it work?

A

Hydroxycarbamide to suppress erythropoiesis.

98
Q

What are the myeloproliferative syndromes?

A

A heterogeneous group of malignant haematopoietic disorders characterised by dysplastic changes in one or more cell lineages, ineffective haematopoiesis and a variable predilection to development of AML>

99
Q

What are the risk factors for myeloproliferative disorders?

A
  • Increasing age
  • Previous cancer therapy esp. radiotherapy and alkylating agents.
  • Environmental toxins
  • Some rarer genetic disorders
100
Q

How do MPDs present?

A

With symptoms of anaemia, neutropenia, and thrombocytopenia.

101
Q

What signs would a pt with MPDs have on examination?

A
  • Petechiae
  • Ecchymoses
  • Pale conjunctivae
  • Signs of heart failure
  • Tachycardia
  • Candidia infection
  • Splenomegaly/lymphadenopathy (uncommon)
102
Q

What are some important differentials to rule out in suspected MPDs?

A
  • Other causes of anaemia (b12/folate/iron def, CKD, haemolysis)
  • Other causes of neutropenia (viral infection, drugs)
  • CML
  • Bone marrow failure
103
Q

How are MPDs diagnosed?

A

By excluding all other causes of cytopaenias.

104
Q

How are MPDs managed?

A

Supportive/symptomatic Rx

High-intensity chemotherapy for otherwise fit and well pts.

105
Q

What are the complications associated with MPDs?

A
  • Complications of anaemia/thrombocytopenia/neutropenia
  • Transfusion dependence
  • Iron overload after transfusion
  • Transform to AML
  • Splenomegaly and spleen complications
106
Q

What is CLL?

A

Chronic lymphocytic leukaemia is a malignant monoclonal expansion of B lymphocytes with abnormal lymphocytes in the blood/bone marrow/spleen etc.

107
Q

How do CLL leukaemia cells appear on blood smear?

A

Mature and small with a narrow border of cytoplasm and dense nucleus.

108
Q

How common is CLL?

A

Most common leukaemia in the Western world.

109
Q

Who is usually affected by CLL?

A

People over age 80

110
Q

Can CLL be inherited?

A

No, but there is a strong familial basis.

111
Q

How might CLL present?

A

Insidious onset of increasing susceptibility to infection, bleeding or petechiae, tiredness and fatigue.

112
Q

What are the signs of CLL?

A
  • Local/generalised lymphadenopathy
  • Splenomegaly
  • Hepatomegaly
  • Petechiae
  • Pallor
113
Q

What differentials are there for CLL?

A

Other leukaemias, lymphoma, or myeloproliferative disorders.

114
Q

A 74 year old man comes to the GP with a 6 month history of increasing tiredness, chronic infections, and now he can feel a mass in his abdomen.

What tests should be done as leukaemia is suspected?

A
  • FBC
  • Peripheral blood smear
  • Bone marrow aspirate
  • Lymph node biopsy

Cancer Care Block (10 decks)

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