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haematology > Malignancies > Flashcards

Malignancies Flashcards

1
Q

What is leukaemia

A

A group of blood cancers associated with an increase in white blood cells

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2
Q

Acute lymphoblastic leukaemia

A

Malignant disease of primitive lymphoid cells (lymphoblasts)

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3
Q

When does acute lymphoblastic leukaemia usually present

A

Children 2-4 years old

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4
Q

What is ALL associated with

A

Downs syndrome

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5
Q

What genetic indicator is associated with ALL and CML

A

Philadelphia chromosome

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6
Q

Pathophysiology of ALL

A

Excessive proliferation of of lymphoblasts leading to pancytopenia

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7
Q

Clinical presentation of ALL

A

Bone pain
Anaemia
Infections
Bleeding

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8
Q

Blood count and film in ALL

A

Reduction in normal cells
Excess leukoblasts

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9
Q

Investigations done for acute leukaemia

A

FBC and film
Coagulation screen
Bone marrow aspirate

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10
Q

Management of acute leukaemia

A

Multi-agent chemotherapy

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11
Q

What is used for long term central venous access in ALL

A

Hickman line

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12
Q

Complications of acute leukaemia

A

Anaemia
Neutropenia
Thrombocytopenia

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13
Q

Consequences of neutropenia

A

Increased severity and duration of infections
Susceptible to fungal infections

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14
Q

Complications of chemotherapy

A

N+V
hair loss
Liver and renal dysfunction
Infection
Infertility

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15
Q

What is acute myeloid leukaemia

A

A malignant disease of primitive myeloid cells

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16
Q

When does acute myeloid leukaemia usually present

A

In the elderly, >60s

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17
Q

Characteristic presentation of acute promyelocytic leukaemia

A

Coagulation defect, DIC

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18
Q

Clinical presentation of AML

A

Similar to ALL, marrow failure

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19
Q

Blood count and film in AML

A

Reduction in normal cells
Excess of myeloblasts

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20
Q

In what type of leukaemia do we see auer rods on blood film

A

AML

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21
Q

Tumour lysis syndrome

A

The release of large amounts of cellular components into the blood stream leading to metabolic disturbances

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22
Q

What causes tumour lysis syndrome

A

Chemotherapy- rapid destruction of cancer cells

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23
Q

Chronic myeloid leukaemia

A

Proliferation of myeloid cells

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24
Q

Gene associated with CML

A

BCR-ABL1

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25
Q

What does the new gene in CML do

A

A tryrosine kinase which causes abnormal phosphorylation leading to haematological changes

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26
Q

What are the 3 phases of CML

A

Chronic phase
Accelerated phase
Blast phase

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27
Q

How long does the chronic phase of CML last

A

5 years

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28
Q

What happens in the chronic phase of CML

A

Excessive proliferation with maturation of the myeloid lineage

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29
Q

When does the accelerated phase of CML occur

A

When the abnormal blast cells take up a high proportion of cells in the bone marrow

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30
Q

How do patients present in the chronic phase of CML

A

Asymptomatic with a raised white cell count

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31
Q

How do patients present in the accelerated phase of CML

A

Develop anaemia, thrombocytopenia and become immunocompromised

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32
Q

What happens in the blast phase

A

Involves an even higher proportion of blast cell >30%

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33
Q

How do patients present in the blast phase of CML

A

More severe symptoms
Pancytopenia

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34
Q

General presentation of CML

A

Hepatomegaly
Hypermetabolic symptoms
Gout

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35
Q

Why can CML cause gout

A

High cell turnover rate giving a high urate

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36
Q

FBC of a patient with CML

A

Normal or decreased Hb
Increased WBC
Platelets variable

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37
Q

Blood film of a patient with CML

A

Leukocytosis with neutrophilia

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38
Q

Further test done specifically for CML and positive result

A

REDUCED leukocyte alkaline phosphatase

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39
Q

What would a bone marrow biopsy show in CML

A

Increased cellularity with increased granulocytes

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40
Q

Management of CML

A

Tyrosine kinase inhibitors

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41
Q

Give an example of a TKI

A

Imatinib

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42
Q

MOA of imatinib

A

Prevents the action of the BCR-ABL fusion protein

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43
Q

What is chronic lymphocytic leukaemia

A

A malignant lymphoproliferative disorder of the mature B lymphoid compartment

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44
Q

When does CLL usually present

A

70s

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45
Q

What organs are usually involved in CLL

A

Lymph nodes
Spleen
Liver

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46
Q

Non-specific symptoms of CLL

A

Night sweats, fever, fatigue, weightloss

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47
Q

Clinical presentation of CLL

A

Often asymptomatic
Lymph node or spleen enlargement
Immunocompromise

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48
Q

FBC results in CLL

A

Hb normal or low
Raised WCC (may be very high)
Platelets normal or low

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49
Q

Blood film in CLL

A

Increased lymphocytes
Smudge/smear cells

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50
Q

How do smudge cells occur

A

Fragile white blood cells rupture during preparation of the blood film and leave a smudge

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51
Q

Bone marrow biopsy results in CLL

A

Heavily infiltrated with lymphocytes

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52
Q

Immunophenotyping in CLL

A

CD19/20 and CD5

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53
Q

Genetic testing in CLL

A

TP53

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54
Q

Indications for treatment of CLL

A

Weight loss of more than 10% in 6 months
Night sweats for longer than 1 month
Progressive marrow failure

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55
Q

What is a complication of CLL

A

Can transform into high grade lymphoma

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56
Q

What is lymphoma

A

Group of cancers that affect the lymphocytes inside the lymphatic system

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57
Q

What is the main clinical sign of lymphoma

A

LYMPHADENOPATHY

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58
Q

What causes Hodgkin lymphoma

A

Proliferation of lymphocytes

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59
Q

When do people usually present with lymphoma

A

Bimodal age distribution
20 and 75 years

60
Q

Risk factors for Hodgkin lymphoma

A

Immunosuppression
Autoimmune disorders
EBV
Family history

61
Q

Give 2 examples of autoimmune conditions that can cause Hodgkin lymphoma

A

Rheumatoid arthritis
Sarcoidosis

62
Q

What is Burkitt lymphoma associated with

A

EBV, HIV and malaria

63
Q

What is associated with MALT lymphoma

A

H.pylori infection

64
Q

What is MALT lymphoma

A

Mucosa associated lymphoid tissue lymphoma

65
Q

Where does MALT lymphoma usually occur

A

Stomach

66
Q

How does diffuse large B cell lymphoma generally present

A

Rapid growing, painless mass in patients over 65

67
Q

Risk factors for non-Hodgkin lymphoma

A

Infections
Hepatitis B or C infection
Exposure to pesticides and trichloroethane
Family history

68
Q

Pain in lymph nodes when they drink alcohol

A

Hodgkin lymphoma

69
Q

How do lymph nodes feel in lymphoma

A

Non tender and rubbery

70
Q

B symptoms of lymphoma

A

Fever, night sweats, fatigue and weight loss

71
Q

Itch without a rash

A

Hodgkin lymphoma

72
Q

Blood test that is raised in Hodgkin lymphoma

A

Lactate dehydrogenase

73
Q

What blood tests are associated with poor outcome of HL

A

Elevated ESR
decreased Hb

74
Q

Diagnostic investigation for lymphoma

A

Lymph node biopsy

75
Q

Key finding from lymph node biopsy in HL

A

Reed-sternberg cells

76
Q

What are reed-sternberg cells

A

Abnormally large B cells that have multiple nuclei that have nucleoli inside them

77
Q

What investigation is used for staging lymphoma

A

CT, MRI and PET

78
Q

What system is used to classify Hodgkin lymphoma

A

Ann-arbor system

79
Q

General management of lymphoma

A

Multi-agent chemo +/- radiotherapy

80
Q

What chemo regiment is used to treat Hodgkin

A

ABVD regiment

81
Q

Drugs in the ABVD regiment

A

Adriamycin
Bleomycin
Vinblastine
Dacarbazine

82
Q

Complication of bleomycin

A

Pneumonitis

83
Q

Long term complications of chemo management of HL

A

Secondary cancer
CVD
infertility

84
Q

Alternative management of HL for patients not responding to chemo

A

Immunotherapy or stem cell transplantation

85
Q

Chemo regiment used in non-Hodgkin lymphoma

A

R-CHOP

86
Q

Drugs in R-CHOP regiment

A

Rituximab
Cyclophosphamide
Hydroxydaunorubicin
Vincristine (oncovin)
Prednisolone

87
Q

Alternative management for patients with NHL not responding to chemo

A

High dose therapy with autologous stem cell rescue or CART therapy

88
Q

What can be used in emergency management of suspected lymphoma

A

Steroids

89
Q

Complication of using steroids to manage lymphoma before biopsy

A

Can cause necrosis and can distort architecture so it confuses diagnosis

90
Q

What is myeloma

A

Cancer of the plasma cells

91
Q

When does myeloma usually present

A

Around 65 yrs

92
Q

Risk factors for myeloma

A

Male
Black African ethnicity
Family history
Obesity

93
Q

What causes myeloma

A

Genetic mutation causes rapid and uncontrolled multiplication

94
Q

Urinalysis of a patient with myeloma

A

Bence jones protein

95
Q

Type of Ig that is usually found in abundance in a patient with myeloma

A

IgG

96
Q

Direct tumour cell effects of myeloma (4)

A

Bone lesions
Increased calcium
Bone pain
Marrow failure

97
Q

Where are lytic lesions usually found in myeloma

A

Spine, skull, long bones and ribs

98
Q

Paraprotein mediated effects of myeloma (4)

A

Renal failure
Immunosuppression
Hyper viscosity
Amyloid

99
Q

Myeloma renal disease

A

Free light chain secretion leads to deposition in the renal tubules causing impairment by cast nephropathy

100
Q

Symptoms of hypercalcaemia

A

Stones
Abdominal groans
Bones
Psychiatric moans

101
Q

Clinical feature associated with myeloma

A

Bone pain (most commonly back pain)

102
Q

Initial investigations used in suspected myeloma

A

Bloods, serum protein electrophoresis, plain x-ray of symptomatic areas

103
Q

Why do we use serum protein electrophoresis

A

To show the type of paraprotein present

104
Q

Diagnostic tests for suspected myeloma

A

Bone marrow aspirate and trephine biopsy
Immunofixation of serum and urine
Whole body MRI

105
Q

Management of myeloma

A

Currently seen as an incurable chronic disease, treatments aim to improve QOL

106
Q

Treatment option for young patients with myeloma

A

Haematopoietic stem cell transplant

107
Q

What can we use to measure response to chemo in myeloma

A

Paraprotein level

108
Q

Combination chemo used in myeloma

A

Corticosteroids: dexamethasone
Novel agents: lenalidamide
MAB: daratumumab
Alkylating agent: cyclophosphamide

109
Q

Symptom control in myeloma

A

Opiate analgesia
Local radiotherapy
Bisphosphonates
Vertebroplasty

110
Q

Why do we use bisphosphonates in myeloma

A

Corrects hypercalcaemia and bone pain by inhibiting osteoclasts

111
Q

What does a vertebroplasty involve

A

Inject sterile cement into fractured bone to stabilise

112
Q

What is lymphadenopathy

A

Enlarged lymph nodes

113
Q

What are the 2 general causes of of lymphadenopathy

A

Reactive and non reactive

114
Q

Give some examples of reactive causes of lymphadenopathy

A

Bacterial infections
Viral infections
Inflammatory conditions
Vaccination

115
Q

List some non-reactive causes of lymphadenopathy

A

Lymphomas
Metastatic cancer
Leukaemia
TB
Idiopathic
Amyloidosis

116
Q

What causes painful lymphadenopathy

A

Reactive causes

117
Q

When might enlarged lymph nodes be rubbery/soft

A

Lymphoma

118
Q

When might the lymph node surface be irregular

A

Metastatic carcinoma

119
Q

What are the 5 main things we can do to investigate lymph node pathology

A

Histology
Immunochemistry of solid node
Immunophenotyping of blood/marrow
Genetic analysis
Molecular analysis

120
Q

What do we use for genetic analysis of a lymph node

A

Fluorescent in situ hybridisation

121
Q

Why do we use genetic analysis of lymph nodes

A

Identify specific patterns of chromosome abnormality in certain lymphomas

122
Q

What happens in idiopathic myelofibrosis

A

Healthy bone marrow is replaced by fibrosis resulting in the lack of production of normal cells

123
Q

When does idiopathic myelofibrosis usually present

A

65

124
Q

Clinical presentation of idiopathic myelofibrosis

A

**can be asymptomatic
Marrow failure
Extra-medullary Haematopoiesis
Hypercatabolism

125
Q

How does extra-medullary Haematopoiesis present

A

Hepatosplenomegaly

126
Q

How does hyper catabolism present

A

Night sweats, extreme weight loss

127
Q

Blood film in idiopathic myelofibrosis

A

Leucoerythroblastic film appearance
Tear drop shaped RBCs in peripheral blood

128
Q

Name the 3 causes of leucoerythroblastic blood film

A

Reactive
Marrow infiltration
Myelofibrosis

129
Q

What are the 3 genes associated with idiopathic myelofibrosis and essential thrombocythaemia

A

JAK2
CALR
MLP

130
Q

Bone marrow biopsy in idiopathic myelofibrosis

A

Dry aspirate
Fibrosis on trephine biopsy

131
Q

Supportive management of idiopathic myelofibrosis

A

Blood transfusions, antibiotics, platelets

132
Q

What can you give to patients with a JAK2 mutation

A

JAK2 inhibitors

133
Q

Name a JAK2 inhibitor

A

Ruxolitinib

134
Q

What is essential thrombocythaemia

A

Uncontrolled production of abnormal platelets

135
Q

When does essential thrombocythaemia usually present

A

65

136
Q

Clinical presentation of essential thrombocythaemia

A

**asymptomatic
Increased cellular turnover
Marrow failure
Thrombosis
Bleeding
Splenomegaly

137
Q

How do we exclude CML when suspecting essential thrombocythaemia

A

Patient will be BCR-ABL1 negative

138
Q

Management of essential thrombocythaemia

A

Aspirin + cytoreductive therapy to control proliferation

139
Q

Give some examples of cytoreductive therapy

A

Hydroxycarbamide
Anagrelide
Interferon alpha

140
Q

What genetic mutation is associated with polycythaemia Vera

A

JAK2

141
Q

How does a mutation in JAK2 cause polycythaemia Vera

A

Results in the loss of autoinhibition
Activation of erythropoeisis in the absence of a ligand

142
Q

What is aquagenic puritis

A

Itch that is worse after a hot shower or bath

143
Q

What is aquagenic puritis associated with

A

polycythaemia Vera

144
Q

FBC and blood film results for a patient with polycythaemia Vera

A

High Hb with erythrocytosis

145
Q

What is erythrocytosis

A

A true increase in red cell mass

146
Q

Management of polycythaemia Vera

A

Venesect to haematocrit <0.45
Aspirin
JAK inhibitor
Cytotoxic oral chemo

haematology (11 decks)

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