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Year 4 Cancer Care and Haem > Haematology > Flashcards

Haematology Flashcards

1
Q

Define Multiple Myeloma

A

Malignant disorder of plasma cells (mature B) characterised by excess secretion of monoclonal antibody

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2
Q

The pathophysiology of Multiple Myeloma involves a two step process. What is the first step?

A

MGUS development

Initial cytogenic abnormality occurs (normally an abnormal response to antigen) which leads to a plasma cell clone

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3
Q

What does MGUS stand for?

A

Monoclonal Gammomopathy of unknown significance

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4
Q

The pathophysiology of Multiple Myeloma involves a two step process. What is the second step?

A

MGUS to MM

Further cytogenic abnormalities occur and changes to marrow microenvironment occur, promoting proliferation

Bone marrow infiltration and excess light chain

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5
Q

What occurs in between the first and second step of myeloma?

A

Pre malignant state called Asymptomatic Myeloma

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6
Q

The presentation of Myeloma can be memorised as ‘CRAB’. Define it

A

Calcium levels high
Renal Impairment
Anaemia
Bone Disease

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7
Q

Define the ‘Calcium’ part of the Myeloma CRAB mnemonic

A

Myeloma induced bone mineralisation
Levels>2.9mmol/l is urgent

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8
Q

Define the ‘Renal Dysfunction’ part of the Myeloma CRAB mnemonic

A

Light chain nephropathy causes increased creatinine

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9
Q

Define the ‘Anaemia’ part of the Myeloma CRAB mnemonic

A

Normal bone marrow destroyed by proliferation of plasma cells
Renal disease reduces EPO

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10
Q

Define the ‘Bone Disease’ part of the Myeloma CRAB mnemonic

A

Wide spread due to disease proliferation
Seen as lytic lesions
Can lead to fractures

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11
Q

Other than the CRAB mnemonic, state three possible presentations of Myeloma

A

Recurrent bacterial infection
Weight Loss
Hyperviscocity Syndrome

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12
Q

How does Hyperviscocity Syndrome (common to MM) present?

A

Blurred vision
Headaches
Mucosal bleeding
Dyspnoea (secondary to HF)

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13
Q

How is Hyperviscocity Syndrome managed?

A

Urgent Plasma Exchange

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14
Q

What age group is typically affected by Multiple Myeloma?

A

Rare in under 40s
Usually over 60s

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15
Q

What is the aim of screening for Multiple Myeloma?

A

Looking for MABs which are the secretion product of malignant clones, using protein electrophoresis and immunofixation

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16
Q

What types of antibodies are normally involved in Multiple Myeloma

A

Normally IgA or IgG

If IgM - suggests Waldenstrom Macroglobulinaemia

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17
Q

Describe the use of Electrophoresis in screening for Multiple Myeloma

A

Separates different proteins into bands using electric current
Band patterns can be normal, polyclonal or monoclonal

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18
Q

Describe the use of Immunofixation in screening for Multiple Myeloma

A

Qualitative and fixes proteins in place using antibodies

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19
Q

What is the assumption in using Electrophoresis to screen for MM?

A

Assumes that the Myelomas secrete intact antibodies

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20
Q

What are light chains and what is the relevance in Multiple Myeloma?

A

Light chains are secreted in normal individuals when monoclonal cells produce more light chains than heavy

The ratio between Kappa and Lambda light chains is the most important (elevated? - myeloma)

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21
Q

What is Urine Electrophoresis used for in Multiple Myeloma?

A

Light chains in the serum may have been filtered by the kidney into the urine

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22
Q

What are light chains found in the urine called?

A

Bence Jones Protein

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23
Q

What would the investigations show if a patient had a non secreting Multiple Myeloma

A

Electrophoresis and Serum Light Chains Negative

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24
Q

Name three broad investigations in order to diagnose Multiple Myeloma

A

Monoclonal Antibody detection
Bone Marrow Aspirate and Trephine with Cytogenetics
Assess organ damage

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25
Q

Describe the diagnostic criteria for MGUS

A

Low monoclonal protein
Bone marrow plasma cells < 10%

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26
Q

Describe the diagnostic criteria for pre malignant Asymptomatic Myeloma

A

Monoclonal protein >3g/dl
Bone marrow plasma cells >10%
No organ damage

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27
Q

Describe the diagnostic criteria for Multiple Myeloma

A

Monoclonal protein present
Bone marrow plasma > 10%
Signs of organ damage

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28
Q

What is the aim of treatment for Multiple Myeloma?

A

Incurable condition
Aim to increase periods of remission

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29
Q

There are four main areas of management for Multiple Myeloma. What is Induction Therapy?

A

Combination of three drugs (Velcade, Revlimid, Dexamethasone)

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30
Q

There are four main areas of management for Multiple Myeloma. What is Autologous Stem Cell Therapy?

A

Provides the best option for long term remission

Stem cells mobilised, harvested and stored following induction

High dose chemotherapy

Stem cells then reinfused

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31
Q

There are four main areas of management for Multiple Myeloma. What is Maintenance Therapy?

A

Bortezamid or Lenalidomide

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32
Q

There are four main areas of management for Multiple Myeloma. What is Relapse Therapy?

A

ASCT/previous regimen or a new therapy

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33
Q

Name four complications of Multiple Myeloma

A

Bone Disease
Hypercalcaemia
Cord Compression
Renal Impairment

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34
Q

What two parameters contribute to the International Staging System for Myeloma?

A

Beta 2 Microglobin
Albumin

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35
Q

What do Pluripotent Stem Cells first specialise into?

A

Myeloid Stem Cells
Lymphoid Stem Cells

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36
Q

What can Myeloid Stem Cells eventually specialise into?

A

Neutrophils
Eosinophils
Basophils
Monocyes
Platelets
Erythrocytes

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37
Q

What do Lymphoid Stem Cells develop into?

A

Blast Cells and then Lymphocytes

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38
Q

Define Acute Myeloid Leukaemia

A

Malignant transformation and proliferation of myeloid progenitor cells
Rare, more common in over 60s

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39
Q

Give four possible aetiologies for AML

A

Myelodysplastic Syndromes
Downs Syndrome
Radiation Exposure
Previous Chemotherapy

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40
Q

Describe the pathophysiology of AML

A

Genetic changes in myeloid progenitor cells lead to proliferation of immature cells unresponsive to normal control mechanisms
Reduced production of normal haematopoietic cells

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41
Q

AML can present with signs of Marrow Failure or Tissue Infiltration. Give three signs of marrow failure

A

Anaemia
Neutropenia
Thrombocytopenia

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42
Q

AML can present with signs of Marrow Failure or Tissue Infiltration. Give three signs of tissue infiltration

A

Lymphadenopathy
Hepatosplenomegaly
Bone Pain

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43
Q

AML can also cause Leucostasis. How would this present?

A

Altered Mental State
Headache
Breathlessness
Visual Changes

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44
Q

What is characteristic on a blood test for AML?

A

Thrombocytopenia
Normocytic Normochromic Anaemia
Raised white cells (maybe lymphopenia)
Raised LDH

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45
Q

What is characteristic on a blood smear for AML?

A

Auer Rods (pink lines)

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46
Q

What is characteristic on a Bone Marrow Aspiration for AML?

A

Myeloid Blast count of >20%

Cytogenetics, Immunophenotyping and Flow Cytometry carried out

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47
Q

What are the principles of AML management?

A

Managed in specialist centres
Enrolled into Clinical Trials
Monitor for infections and coagulopathy
Cytoreduction with Hydroxycarbamide

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48
Q

What should be anticipated with AML treatment?

A

Tumour Lysis Syndrome

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49
Q

How is AML Chemotherapy set up?

A

Induction (Intense) and Consolidation cycles

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50
Q

What other treatment could you consider for AML?

A

ASCT

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51
Q

Give four poor prognostic factors for AML

A

Age>60
Multiple Comorbidities
Previous Haematological Disorders
Previous Exposure to Chemoradio

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52
Q

Define CML

A

Chronic Myeloid Leukaemia

Abnormal clonal expansion of cells in myeloid lineage, most common in 50s and 60s

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53
Q

Describe the genetics of CML

A

Reciprocal translocation between chromosomes 9 and 22
Creates Philadelphia chromosome
Fusion of BCRABL genes
Promotes production of Tyrosine Kinase

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54
Q

CML can be asymptomatic. If not, how could it present?

A

Splenomegaly
Fatigue, Weight Loss, Early Satiety
Signs of BM infiltration

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55
Q

What would an FBC for CML show?

A

Marked Neutrophilia
?Basophilia
?Eosinophilia

May show anaemia and thrombocytopenia

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56
Q

What are markers of high cell turnover?

A

LDH
Urate
Potassium

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57
Q

What is seen on a blood film of CML?

A

Mixture of immature and mature myeloid precursors

Proportion of blast cells to basophils helps stage

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58
Q

Other than bloods, what investigations are done for CML?

A

Bone Marrow Aspiration +/- Trephine
Identifying Philadelphia chromosome

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59
Q

How is the Philadelphia Chromosome identified?

A

Metaphase Cytogenetics

FISH/Reverse Transcriptase PCR can determine presence of BCRABL

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60
Q

There are three different phases in CML. Describe the Chronic Phase

A

Non Specific symptoms (fatigue, night sweats, weight loss)
Without treatment, this phase lasts 3-5 years

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61
Q

There are three different phases in CML. Describe the Accelerated Phase

A

Symptoms and features are more apparent and severe
If untreated, phase lasts 6-18 months
Blast Cells 15-29%
Basophils>20%
Persistent thrombocytopenia

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62
Q

There are three different phases in CML. Describe the Blast Phase

A

Rapid expansion of blasts, without treatment survival is a few months
Blasts>30%
Extramedullary blast proliferation

63
Q

Describe three management options for CML

A

Tyrosine Kinase Inhibitors - to directly block enzyme produced by BCRABL
Intensive Chemotherapy - same as AML
ASCT - for chronic phase relapse

64
Q

Name a first generation Tyrosine Kinase inhibitor

A

Imatinib

65
Q

Name two other Tyrosine Kinase inhibitors

A

Dasatinib
Nilotinib

66
Q

How should Chronic Phase CML patients be managed?

A

If WCC>100 then cytoreduction
Oral Hydration and Allopurinol
First line - Imatinib

67
Q

How is Advanced Phase CML managed?

A

Ideally patients should be enrolled onto a clinical trial

Second generation TKI with or without Chemotherapy

68
Q

What is the survival rate of CML?

A

15-64 has a 90% 5 year survival
>65 has a 40% 5 year survival

69
Q

Define Acute Lymphoblastic Leukaemia

A

Most common malignancy of childhood

Lymphoid progenitor cells undergo malignant transformation (mostly B)

Clonal expansion causes lymphoid precursors to replace normal cells

70
Q

At what age does ALL incidence peak?

A

0-4

71
Q

What is the aetiology of ALL?

A

Poorly understood

Thought to be a genetic predisposition and a trigger (such as a virus)

72
Q

Name three cytogenic abnormalities in ALL

A

12:21 translocation
9:22 translocation (Philadelphia)
4:11 translocation

73
Q

How does ALL normally present?

A

Normally a short history of marrow supression or lymphadenopathy
Marrow Failure, Tissue Infiltration, Leucostasis

74
Q

How is ALL investigated?

A

FBC
Imaging - CXR/CT
BM Aspirate and Biopsy

75
Q

Give three poor prognostic factors of ALL

A

Age (worse with advancing age)
Performance Status>1
CNS involvement

76
Q

What should be done pre ALL management?

A

Steroids, IV Hydration and Allopurinol to prevent Tumour Lysis Syndrome
Anaemia and Thrombocytopenia mx
G-CSF for Neutropenia

77
Q

What is the aim of induction therapy in ALL?

A

Aim to achieve complete remission, or ideally complete molecular remission

78
Q

What is Complete Remission in ALL?

A

Leukaemia not seen in bone marrow, CSF or Peripheral Blood

79
Q

What is Complete Molecular Remission in ALL?

A

Minimal residual disease not detectable by sensitive molecular probe

80
Q

What is the maintenance therapy for ALL?

A

Reduce recurrence risk
Daily 6 Mercaptopurine and weekly methotrexate

81
Q

Give three complications of ALL

A

Neutropenic Sepsis
Tumour Lysis Syndrome
SVCO

82
Q

Define Chronic Lymphocytic Leukaemia

A

Lymphoproliferative disorder of B lymphoyctes leading to widespread lymphadenopathy and secondary complications
Most common form of Leukaemia in adults in western world

83
Q

Describe the pathophysiology of CLL

A

Initial alterations causes pre malignant monoclonal B cell lymphocytosis
Further genetic and bone marrow transformation allows change to CLL

84
Q

How does CLL present?

A

Can be asymtomatic and remain stable for many years, or can have aggressive form and deteriorates quickly

Typical B symptoms
Lymphadenopathy
Hepatomegaly
Splenomegaly

85
Q

What is diagnostic of CLL?

A

Absolute B lymphocyte count >5 for more than 3 months

With a characteristic immunophenotype

86
Q

What is a complication of CLL?

A

Autoimmune Haemolytic Anaemia

87
Q

What is seen on a blood film of CLL?

A

Lymphocytosis and Smudge/Smear cells (caused by damage to lymphocytes in preparation)

88
Q

Why is Flow Cytometry used in CLL?

A

Shows its due to a clonal lymphocyte

89
Q

When would you consider doing a Bone Marrow aspiration, or imaging in CLL?

A

If an alternative diagnosis was suspected

90
Q

There are two possible stagings for CLL. Describe the Binet Staging

A

A - <3 lymphoid sites
B - >3 lymphoid sites
C - Presence of anaemia/thrombocytopenia

91
Q

There are two possible stagings for CLL. Describe the Rai Staging

A

0 - Lymphocytosis
I-II - Lymphocytosis, Lymphadenopathy and Organomegaly
III-IV - Anaemia and Thrombocytopenia

92
Q

Give three prognostic indicators in CLL

A

Lymphocyte doubling time
Genetic Abnormalities
Beta 2 microglobulin

93
Q

What is Watch and Wait management for CLL?

A

For asymptomatic patients with low stages

3 monthly bloods

94
Q

Give four indications for management in CLL

A

Bone Marrow Failure
Lymphadenopathy
Progressive Lymphocytosis
Autoimmune complications

95
Q

How is CLL managed?

A

Two different regimens each containing three chemotherapy agents
Which one depends if TP53 mutation is present

96
Q

Give an example of a chemotherapy drug used in CLL

A

Chlorambucil (cross links DNA)

97
Q

Give an example of a small molecule drug used in CLL

A

Ibrutinib (Tyrosine Kinase Inhibitor)

98
Q

Give an example of a monoclonal antibody used in CLL

A

Rituximab

99
Q

Other than chemotherapy, what treatment should be considered in CLL?

A

ASCT
Vaccinations
Steroids

100
Q

Name three complications of CLL

A

Richter transformation (formation of agressive lymhpoma with rapid deterioration)
Secondary infections
Hyperviscocity Syndrome

101
Q

Define Hodgekin’s Lymphoma

A

Rare malignancy of bimodal distribution, peaking at 20-30 and again at older age

102
Q

Describe the aetiology of Hodgekin’s Lymphoma

A

Cause unknown
Links to Immunosupression, EBV, HIV, Smoking

103
Q

There are two main types of Hodgekin’s Lymphoma, what are they?

A

Classical
Nodular

104
Q

What are the four subtypes of Hodgekin’s Lymphoma?

A

Nodular Sclerosis
Mixed Cellularity
Lymphocyte Rich
Lymphocyte Depleted

105
Q

Describe the pathophysiology of Classical HL

A

Characteristic binucleate Reed Sternberg Cells (Owls)

Infiltrating cells are T Regulator cells

106
Q

Describe the pathophysiology of Nodular HL

A

Characterised by L and H Hodgekin Cells (aka Popcorn Cells)
Can run a relapsing and remitting course

107
Q

How does Hodgekin’s Lymphoma present?

A

Painless rubbery lymphadenopathy
B Symptoms
Itch
Alcohol induced LN pain

May have hepatosplenomegaly or mediastinal mass

108
Q

What are B symptoms?

A

Unexplained Fever
Unexplained Night Sweats
>10% Weight Loss in 6m

109
Q

How do you diagnose Hodgekin’s Lymphoma?

A

Excisional Biopsy of Lymph Nodes

110
Q

What other investigations are recommended in HL?

A

PET CT
Bloods
CXR/MRI (spread dependent)

111
Q

What is the problem with using a PET CT for Hodgekin’s Lymphoma?

A

Negative Predictive Value is high

Long term monitoring is not recommended due to false positives

112
Q

Give three features indicating a poor Hodgekin’s prognosis

A

Albumin <40
Male
Lymphocytes<0.08

113
Q

The treatability of Hodgekin’s Lymphoma is good, the issue is the toxicities of treatment. Name three

A

Secondary Malignancies
Fibrosis
Coronary Artery Disease

114
Q

How is early stage Hodgekin’s Lymphoma managed?

A

2-4 cycles of ABVD chemotherapy, and radiotherapy

115
Q

What is the ABVD chemotherapy regime?

A

Doxorubicin (Inhibits DNA synthesis)
Bleomycin (Inhibits DNA synthesis)
Vinblastine (Inhibits microtubule formation)
Decarbazine (Alkylating agent)

116
Q

How is advanced stage Hodgekin’s Lymphoma managed?

A

6-8 cycles ABVD (or other regimes such as BEACOPP)
Radiotherapy

117
Q

How should a Hodgekins Lymphoma relapse be treated?

A

Depends on prognostic indicators and timing

If >12m then salvage therapy (IVE, DHAP, ESHAP)

118
Q

What is important to note on medical records of previous Hodgekin’s Lymphoma patients?

A

Should recieve irradiated blood and platelets for life

119
Q

Define Non Hodgekin’s Lymphoma

A

Spectrum ranges from low grade lymphomas that are incurable but compatible with many years of life to high grade (left untreated are rapidly fatal)

120
Q

Give four possible causes of Non Hodgekin’s Lymphoma

A

Age
Prolonged Immunosupression
EBV
H.Pylori (Gastric)

121
Q

How can Non-Hodgekins Lymphoma be classified?

A

Based on whether lymphomas are B or T cells, percieved origin cell and molecular characteristics

122
Q

There are many different subtypes of Non Hodgekins Lymphoma. Name three

A

Follicular B Cell
Mature B Cell
Leukaemic

123
Q

Describe the characteristics of Low Grade Non Hodgekins Lymphoma

A

Relatively long survival
Incurable (relapsing and remitting)
Non destructive growth patterns
CNS involvement is rare

124
Q

Describe the characteristics of High Grade Non Hodgekins Lymphoma

A

Aggressive clinical course and rapidly fatal without treatment
Curable in a significant proportion
Destructive growth pattern
CNS involvement is common

125
Q

How does Low Grade Non Hodgekins Lymphoma present?

A

Gradual lymphadenopathy
Malaise
Marrow Involvement

126
Q

How does High Grade Non Hodgekins Lymphoma present?

A

Rapidly enlarging mass
B symptoms

End Stage - Ascites and Pleural Effusion

127
Q

Name three places of Extranodal involvement in Non Hodgekins Lymphoma

A

CNS
Cutaneous
GI Tract

128
Q

Name two types of High Grade Non Hodgekins Lymphoma

A

Burkitts
Lymphoblastic

129
Q

How is Non Hodgekins Lymphoma investigated?

A

Lymph Node Biopsy (ideally excisional)
Bloods
Imaging (CXR, CT, PET CT)
Bone Marrow Aspirate

130
Q

What is used to stage Non Hodgekins Lymphoma?

A

CXR
CT
Blood count and film
BM Aspirate
Renal Biochem
Markers of tumour burden

131
Q

What is the Lymphoma staging tool called?

A

Lugano staging

(Limited, Bulky, Advanced)

132
Q

What is the management of Non Hodgekins Lymphoma?

A

R CHOP
Rituximab, Cyclophosphamide, Doxorubicin, Vincristine

Prednisolone

+/- Radiotherapy as adjuvant

133
Q

What is the most common form of NHL?

A

Diffuse Large B Cell

134
Q

What is the second most common form of NHL?

A

Follicular lymphoma

85% have translocations between 14 and 18

135
Q

What is Burkitt’s Lymphoma?

A

High grade rapidly proliferating B cell NHL commonly affecting children
Striongly associated with EBV

136
Q

How does Burkitt’s Lymphoma present?

A

Rapidly enlarging tumour in jaw/neck/abdomen
May have bowel obstruction
May have B symptoms

137
Q

How is Burkitt’s Lymphoma managed?

A

High grade lymphoma so very chemosensitive

Ideally R-BFM regime, but if not then use less intensive R-CHOP

Monitor for Tumour Lysis

138
Q

Name three differences between Acute and Chronic Leukaemias

A

1) Acute Leukaemias have a more rapid onset compared to chronic
2) Acute Leukaemias can have affect children whereas chronic Leukaemias tend to only affect adults
3) Acute Leukaemias are characterised by blast cells on the film whereas Chronic are more well differentiated

139
Q

Give a primary and secondary cause of Polycythaemia

A

Primary - Polycythaemia Ruba Vera
Secondary - Chronic Lung Disease, Dehydrated

140
Q

How could Polycythaemia present?

A

Headaches
Thrombosis
Blurred Vision
Itchy skin after bathing

141
Q

How should Polycythaemia be investigated?

A

Haematocrit
EPO levels (if raised look for phaeochromocytoma or fibroids)
Assess spleen size

142
Q

Describe the first and second line management of Polycythaemia Rubavera

A

First Line - Therapeutic venesection (once the levels are low enough, their ‘treatment’ can be giving blood)

Second Line - Hydroxycarbamide (second due to malignancy risk)

143
Q

What other supportive management is advised for Polycythaemia?

A

75mg Aspirin
Remain well hydrated
Be careful of long haul flights

144
Q

Give four differentials for Essential Thrombocytosis

A

Malignancy
Infection
Inflammation
Post Op

145
Q

Management for essential thrombocytosis depends on risk. Describe this

A

Low risk (<40) - Aspirin
High Risk (>60) - Hydroxycarbamide
Intermediate - clinical judgement

146
Q

Describe the phases of Myelofibrosis

A

Cellular Phase - raised cell count, extramedullary haematopoiesis

Post Cellular Phase - Transfusion dependent, uncomfortable enlarged spleen

147
Q

What is the main concerning complication of Myelofibrosis

A

AML

148
Q

What should you monitor for with respective paraproteinaemias?

A

IgM - Lymphoma (Low Grade Waldenstroms Macroglobulinaemia)

IgA/IgG - Myeloma

149
Q

What are the categories for red cell transfusion?

A

R1 : Acute Blood Loss
R2: Hb <70
R3: Hb<80 (CVS Disease)
R4: Chronic Anaemia (individual threshold)
R5: Maintaining Hb>110 for Radiothefaph
R6: Exchange transfusion

150
Q

Name two causes of spherocytosis

A

Hereditary Spherocytosis
Haemolytic Anaemia

151
Q

Name four categories of immunological complications from transfusion

A

Sensitisation to red cell antigens (immediate or delayed)
Sensitisation to white cell antigens (febrile reaction, TRALI)
Sensitisation to platelet antigens (Post transfusion)
Graft vs host

152
Q

Name three categories of non immunological complications from transfusion

A

Infective disease transmission
Circulatory overload
Transfusion Haemosiderosis

153
Q

What other investigations need to be done in Myeloma?

A

Full body MRI
Bloods
Bone marrow trephine and aspiration

Year 4 Cancer Care and Haem (16 decks)

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