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Year 4 - Cancer Care > 2.02 - Malignant Haematology > Flashcards

2.02 - Malignant Haematology Flashcards

1
Q

What are the broad types of haematological malignancies?

A
  • leukaemia
  • lymphoma
  • myeloma
  • myelodysplastic syndromes
  • myeloproliferative syndromes
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2
Q

Broadly, what is the pathophysiology of haematological malignancy?

A

Loss of normal tight controls of haemopoiesis:
- too many cells proliferating
- cells don’t apoptose
- cells don’t differentiate

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3
Q

What are the myeloid malignancies?

A
  • acute myeloid leukaemia (AML)
  • chronic myeloproliferative neoplasms (MPNs)
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4
Q

What are the lymphoid malignancies?

A
  • acute lymphoblastic leukaemia (ALL)
  • chronic lymphocytic leukaemia (CLL)
  • lymphoma
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5
Q

General presentation of haematological malignancy.

A

Symptoms of bone marrow failure:
- anaemia (tired, SOB, dizziness)
- thrombocytopenia (abnormal bruising or bleeding)
- neutropenia (recurrent infection)

Symptoms of disease involvement:
- lumps
- hepatosplenomegaly

Constitutional symptoms:
- weight loss
- drenching night sweats
- fevers
- intense pruritis

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6
Q

Symptoms of hypercalcaemia.

A
  • fatigue
  • abdominal pain
  • N+V
  • constipation
  • confusion
  • headaches
  • polydipsia
  • polyuria
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7
Q

Hypercalcaemia of unknown cause is investigated as…

A

Myeloma

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8
Q

Symptoms of hyperviscocity.

Can occur in any haematological malignancy.

A
  • headaches
  • visual disturbance
  • sleepiness
  • ischaemic events
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9
Q

Routine bloods to investigate haematological malignancy.

A
  • FBCs
  • U&Es
  • LFTs
  • CRP
  • Ca2+
  • haematinics
  • retics
  • blood film
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10
Q

Special bloods to investigate haematological malignancy.

A
  • LDH & urate (cell turnover)
  • serum free light chains
  • flow cytometry
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11
Q

Imaging to investigate haematological malignancy.

A
  • CT NeckCAP
  • PET scan
  • MRI spine/pelvis
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12
Q

Invasive investigations for haematological malignancy.

A
  • core tissue biopsy
  • bone marrow aspirate and trephine
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13
Q

What is flow cytometry?

A

Identifies classes of cells based upon the pattern of protein expression.

Malignant cells have different protein expressions, therefore will be highlighted on flow cytometry.

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14
Q

What is leukaemia?

A

A malignancy of the bone marrow causing an increase in the number of leukocytes.

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15
Q

How is leukaemia classified?

A
  • myeloid vs lymphoid
  • acute vs chronic
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16
Q

What is acute lymphoblastic leukaemia (ALL)?

A

The acute proliferation of lymphoid blast cells (B or T cells).

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17
Q

Presentation of ALL.

A

Pancytopenia:
- anaemia sx
- thrombocytopenia sx
- neutropenia sx

Bone pain (esp. younger pts)

Lymphadenopathy.

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18
Q

Age distribution of ALL diagnosis.

A

Peak age 0-4 years.

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19
Q

Investigations of ALL.

A
  • FBCs
  • blood film (lymphoblasts)
  • bone marrow biopsy
  • cytogenetics
  • flow cytometry
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20
Q

Role of lumbar puncture in ALL.

A

ALL can migrate to the CSF.

LP can be used to diagnose and introduce chemotherapy into the CSF.

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21
Q

Management of ALL.

A

Multi-drug chemotherapy.

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22
Q

Associations of ALL.

A
  • Down’s syndrome
  • Philadelphia mutation (<20%)
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23
Q

What is acute myeloid leukaemia (AML)?

A

The acute proliferation of the myeloid stem cell or myeloid blast cell.

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24
Q

Precursor of AML.

A
  • polycythaemia vera
  • myelofibrosis
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25
Blood film / bone marrow biopsy findings of AML.
- myeloblasts - Auer rods in cytoplasm
26
Presentation of AML.
Pancytopenia: - anaemia sx - thrombocytopenia sx - neutropenia sx
27
Treatment of AML.
Intensive chemotherapy. Allogenic stem cell transplant.
28
What is the age distribution most commonly affected by AML?
Over 60s.
29
What are the three phases of chronic myeloid leukaemia (CML)?
- chronic phase - accelerated phase - blast phase
30
Presentation of CML.
- leukocytosis (incl. basophilia) - splenomegaly Otherwise usually asymptomatic at time of diagnosis.
31
Genetic mutation associated with CML.
Philadelphia mutation - activates tyrosine kinase pathway. Results in uncontrolled cellular proliferation.
32
Chronic phase of CML.
- asymptomatic - pts diagnosed after incidental leukocytosis - can last several years
33
Accelerated phase of CML.
- blast cells infiltrate bone marrow and blood (<20%) - patients become symptomatic (anaemia, thrombocytopenia, neutropenia)
34
Blast phase of CML.
- higher proportion (>20%) of blast cells in the blood - severe symptoms (pancytopenia) - often fatal
35
Management of CML.
Tyrosine kinase inhibitors can induce remission and give normal life expectancy. Some patients remain in remission OFF medication - potentially curable.
36
What is chronic lymphocytic leukaemia (CLL)?
The slow clonal expansion of a single well-differentiated lymphocyte (usually B lymphocyte).
37
Presentation of CLL.
- asymptomatic - age > 60 years
38
Complications of CLL.
- autoimmune haemolytic anaemia - immune thrombocytopenic purpura
39
What is Richter's transformation?
The rare transformation of CLL into high-grade B-cell lymphoma.
40
Blood film findings associated with CLL.
- smear / smudge cells
41
Management of CLL.
- chemotherapy - targeted immune treatments
42
What are myeloproliferative neoplasms (MPNs)?
The uncontrolled and chronic proliferation of myeloid stem cells.
43
MPNs examples.
- primary myelofibrosis (PMF) - polycythaemia vera (PV) - essential thrombocythaemia (ET)
44
Proliferating cell line in a) PMF b) PV c) ET
a) haematopoietic stem cells b) erythroid cells c) megakaryocytes
45
FBC consistent with PMF.
- anaemia - high or low WCC - high or low platelet count
46
FBC consistent with PV.
- elevated haematocrit
47
FBC consistent with ET
- thrombocytosis
48
Mutations associated with MPNs.
- JAK2 (most commonly) - MPL - CALR
49
Presentation of essential thrombocythaemia.
Thrombosis sx: - headaches - blurred vision - erythromelalgia Haemorrhage. Splenomegaly.
50
Risks of ET.
Transformation to: - myelofibrosis - AML
51
Treatment for ET.
- low dose aspirin - chemotherapy targeting platelets - immunotherapy
52
What is polycythaemia vera (PV)?
JAK2 mutation causes uncontrolled production of red cells in bone marrow, despite EPO production being switched off.
53
Presentation of PV.
Thrombosis sx: - headaches - blurred vision - erythromelalgia Pruritis after a bath. Plethoric complexion.
54
Risks of PV.
- leukaemic transformation - myelofibrosis
55
Investigations for PV.
- FBC - cytogenetics (JAK2) - bone marrow biopsy
56
Treatment of polycythaemia (low risk of thrombosis).
- venesection - low dose aspirin
57
Treatment of polycythaemia (high risk of thrombosis).
- chemotherapy - JAK2 inhibitors - allopurinol
58
Rationale of allopurinol in polycythaemia vera.
High RBC turnover increases uric acid release. Allopurinol lowers the amount of uric acid in the blood, and prevents gout.
59
Secondary causes of thrombocytosis.
- bleeding - iron deficiency - inflammation - infection - post-surgical - splenectomy
60
Secondary causes of polycythaemia.
- chronic hypoxia - smoking - obstructive sleep apnoea - altitude - renal / hepatic tumours (EPO secreting) - congenital heart disease
61
Clinical signs of polycythaemia.
- red face - conjunctival plethora - splenomegaly - hypertension
62
Causes of myelofibrosis.
- primary myelofibrosis - polycythaemia vera - essential thrombocythaemia
63
What is myelofibrosis?
Proliferation of a single cell line leads to bone marrow fibrosis. Fibrosis affects the production of blood cells and leads to: - anaemia - thrombocytopenia - leukopenia
64
Sites of extramedullary fibrosis.
- liver (hepatomegaly) - spleen (splenomegaly) - spine (spinal cord compression)
65
Blood film typical of myelofibrosis.
- teardrop-shaped red blood cells - anisocytosis (varying sizes of red blood cells) - blast cells
66
Risks of myelofibrosis.
Leukaemic transformation.
67
Management of myelofibrosis.
- supportive care - JAK2 inhibitor - splenectomy - bone marrow transplant
68
What is lymphoma?
The clonal proliferation of lymphoid cells, ultimately resulting in lymphadenopathy.
69
What are the types of lymphoma?
- Hodgkin's lymphoma - Non-Hodgkins lymphoma
70
Microscopic findings in Hodgkin's lymphoma.
Reed Sternberg cells
71
Risk factors for Hodgkin's lymphoma.
- HIV - Epstein-Barr virus - autoimmune conditions (e.g. RA, sarcoidosis, SLE) - family history
72
Age distribution of Hodgkin's lymphoma.
20-25 years then 80 years.
73
Types of non-Hodgkin's lymphoma.
- diffuse large B cell lymphoma - Burkitt lymphoma - MALT lymphoma
74
Features of diffuse large B cell lymphoma.
Rapidly growing painless mass, in older patients.
75
Features of Burkitt lymphoma.
Associated with Epstein-Barr virus and HIV.
76
Features of MALT lymphoma.
Affects mucosa-associated lymphoid tissue, around the stomach.
77
Risk factors for non-Hodgkin's lymphoma.
- HIV - Epstein-Barr virus - H. pylori - HBV / HCV - exposure to pesticides - family history
78
Presentation of lymphoma.
Lymphadenopathy: - non-tender - firm - rubbery B symptoms: - fever - weight loss - drenching night sweats Non-specific symptoms: - fatigue - itching - cough - SOB - abdominal pain - recurrent infections
79
Investigations for lymphoma.
- immunohistochemistry - flow cytometry - cytogenetics - karyotyping - lymph node biopsy
80
CD antigens associated with: a) T-cell lymphoma b) B-cell lymphoma
a) CD20 and CD79a b) CD3, CD4 and CD8
81
What is the lymphoma paradox?
82
How is lymphoma classified?
Ann Arbor / Lanugo classification - emphasises whether the affected nodes are above or below the diaphragm.
83
Treatment of Hodgkin's lymphoma.
- chemotherapy - radiotherapy
84
Management of non-Hodgkin's lymphoma.
Depends on the type and stage: - watchful waiting - chemotherapy - monoclonal antibodies - radiotherapy - stem cell transplantation
85
What is myeloma?
A bone marrow malignancy resulting in clonal proliferation of plasma cells.
86
What are paraproteins?
The clonal proliferation of a plasma cell results in the large quantities of a specific paraprotein, which is an abnormal antibody or part of an antibody.
87
What is multiple myeloma?
Where the myeloma affects multiple bone marrow areas in the body.
88
What is monoclonal gammopathy of undetermined significance (MGUS)?
Production of a specific paraprotein without other features of myeloma or cancer. It is an incidental finding in an otherwise healthy person.
89
Risk of progression to myeloma for MGUS.
1%
90
What is smouldering myeloma?
Abnormal plasma cells and paraproteins, but no organ damage or symptoms.
91
Risk of progression to myeloma for smouldering myeloma.
10%
92
Pathophysiology of myeloma.
A genetic mutation in the bone marrow results in the clonal expansion of a single type of plasma cell. This plasma cell produces a specific paraprotein: - IgA - IgG - IgM - IgD - IgE - kappa light chain - lambda light chain
93
Presentation of myeloma.
94
Pathophysiology of anaemia of myeloma.
Bone marrow infiltration results in the suppression of other blood cell lines, leading to: - anaemia - leukopenia - thrombocytopenia
95
What is myeloma bone disease?
Abnormal plasma cells release cytokines that promote osteoclast activity, and suppress osteoblast activity. This results in bone resorption, AKA osteolytic lesions. These lesions are at risk of pathological fractures. It also causes hypercalcaemia.
96
What is a plasmacytoma?
Individual tumours formed by cancerous plasma cells, occurring in bones or soft tissue.
97
What are the common sites of myeloma bone disease?
- skull - spine (vertebral fracture) - long bone - ribs
98
What are the causes of renal disease in myeloma?
- paraprotein deposition in the kidneys - hypercalcaemia - dehydration - glomerulonephritis - medications used to treat the condition
99
What defines myeloma?
100
Risk factors for myeloma.
- older age - male - black ethnic origin - family history - obesity
100
What is hyperviscocity syndrome?
Clonal expansion of paraproteins increases plasma viscocity, causing a haematological malignancy. It can cause complications: - bleeding - visual symptoms - retinal haemorrhages - neurological complications (e.g. stroke) - heart failure
101
Laboratory investigations for myeloma.
- FBC (anaemia / leukopenia) - calcium (raised) - ESR (raised) - plasma viscocity (raised) - U&Es (?renal impairment)
102
Specialist laboratory investigations for myeloma.
- serum protein electropheresis - serum free light chain assay - urine protein electropheresis
103
What is the role of serum protein electropheresis in the diagnosis of myeloma?
Detects paraproteinaemia. ie. heavy chains (IgA, IgG, IgM, IgD or IgE)
103
What is the role of serum-free light-chain assay in the diagnosis of myeloma?
Detects abnormally abundant light chains.
103
What is the role of urine protein electropheresis in the diagnosis of myeloma?
Detect Bence-Jones protein
104
What light chains do plasma cells produce? Give the normal ratio.
Kappa:Lambda 2:1 ratio
105
Diagnostic test for myeloma.
Bone marrow biopsy.
106
Imaging used in myeloma.
- whole-body MRI - whole-body low-dose CT NB: NOT skeletal survey.
107
X-ray findings consistent with myeloma.
- well-defined lytic lesions - diffuse osteopenia - abnormal fractures Raindrop skull / pepper-pot skull refers to multiple lytic lesions seen in the skull on an x-ray.
108
What is amyloidosis?
The extracellular tissue deposition of fibrils - commonly affects renal, liver, heart, gastrointestinal tract or peripheral nerves.
109
Management of myeloma.
Chemotherapy to induce remission. Stem cell transplant may be an option for fitter patients.
110
Define stem cell transplant a) autologous b) allogenic
a) using the person's own stem cells b) using stem cells from a healthy donor
111
Management of myeloma bone disease.
- bisphosphonates - radiotherapy - orthopaedic surgery - cemental augmentation
112
Complications of myeloma.
- infection - bone pain - fractures - renal failure - anaemia - hypercalcaemia - peripheral neuropathy - MSCC - hyperviscocity syndrome - venous thromboembolism
113
What are myelodysplastic syndromes?
A form of cancer caused by a mutation in the myeloid cells in the bone marrow, resulting inadequate haematopoiesis.
114
Progression of myelodysplastic syndromes.
Risk to transform into AML.
115
Presentation of myelodysplastic syndrome.
Patients may be asymptomatic and diagnosed after incidental findings on a FBC. They may present with symptoms of: - anaemia (fatigue, SOB, pallor) - neutropenia (frequent or severe infections) - thrombocytopenia (bleeding and purpura)
115
Diagnosis of myelodysplastic syndromes.
- FBC (anaemia, thrombocytopenia, neutropenia) - blood film (blast cells) - bone marrow biopsy
116
Management of myelodysplastic syndromes.
- watchful waiting - supportive treatment (e.g. blood or platelet transfusion) - erythropoietin (anaemia) - G-CSF (neutropenia) - chemotherapy - targeted therapies - allogenic stem cell transplant

Year 4 - Cancer Care (13 decks)

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