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Haematology Revision > 3 Big: Leukaemias, Lymphomas and Myelomas > Flashcards

3 Big: Leukaemias, Lymphomas and Myelomas Flashcards

1
Q

From what cells does AML form from? Can they continue differentiating?

A

Myeloid progenitor cells

No

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2
Q

In which group of people is AML the MOST common cancer?

A

This is the most common adult cancer

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3
Q

What does AML stand for?

A

Acute Myeloid Leukaemia

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4
Q

What is the cause of AML?

A

Mainly Idiopathic
Can be a complication of chemotherapy for a previous lymphoma(explain the risk to parents)
Myelodysplastic syndrome
Down’s syndrome

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5
Q

What is the MAIN presentation of AML? (3)

A

BONE MARROW FAILURE:
Anaemia
Thrombocytopenia(purpura and mucosal bleeding)
With subconjunctival bleeding and Ecchymosis

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6
Q

What are the clinical features of AML when there is infiltration

A 
Infection due to neutropenia
Splenomegaly
Hepatomegaly 
Gum hypertrophy
CNS symptoms (Rare)
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7
Q

What are the key Investigations for AML?

A 
Blood count and blood film 
Bone marrow aspirate
Cytogenetics 
Immunophenotyping of leukaemia blasts 
CSF examination ie LP
Molecular genetics
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8
Q

What will you see on the blood count and film in AML?

A

Anaemia

Often a raised WCC, but can be same/low, LOW platelets

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9
Q

What is the defining feature of AML on bone marrow aspirate?

A

Myeloid blasts (20%)

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10
Q

What acquired gene mutations are seen in AML?

A

FLT3, ICD = iso citrate dehydrogenase

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11
Q

What are the management options for AML?

A

Supportive treatment
Anti-laeukamic chemotherapy
Allogenic stem cell transplant
All-trans retinoid acid in APL which decreases the DIC risk
Targeted antibodies eg tyrosine kinase inhibitors

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12
Q

What are 2 examples of anti-leukeamic chemotherapy in AML?

A

Daunorubicin

Cytarabine

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13
Q

What is the prognosis if AML?

A

This is a very rapidly progressing disease, but can be cured if caught early enough

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14
Q

What does CML stand for?

A

Chronic Myeloid Leukaemia

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15
Q

Is CML more common in males or females?

A

Malses

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16
Q

When is the peak incidence of CML?

A

40-60yo’s

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17
Q

What percentage of leukaemia does CML make up?

A

15%

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18
Q

What CHROMOSOME is mutated in CML?

A

PHILIDELPHIA CHROMOSOME ( in 95% of people)

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19
Q

What type of mutation gives rise to the philadelphia chromosome?

A

Reciprocal translocation between the chromosome 9 and 22 long arms leading to the fusion of the BCR and All genes on chromosome 22

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20
Q

What does the mutation cause increased activity of in CML?

A

Tyrosine Kinase

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21
Q

Can the cells continue to differentiate in CML?

A

The leukaemia do have the ability to differentiate here, yes!

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22
Q

Is there bone marrow failure in CML?

A

NO!

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23
Q

What are the 3 stages of CML?

A

Chronic - asymptomatic, for years
Accelerated, symptomatic and can’t control blood counts, increased splenomegaly
Blast transformation: features of AML and death

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24
Q

What are the clinical features of CML?

A 
Anaemia 
Night sweats, systemic fever
Splenomegaly
Fatigue
Hyperleukostasis
Gout
NO BONE MARROW FAILURE
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25
Q

What does hyperleukostasis cause?

A

Fundal haemorrhage
Venous congestion
Altered consciousness
Respiratory failure

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26
Q

What investigations are key if you suspect CML?

A

Blood count and blood film

Bone marrow aspirate

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27
Q

What will the blood film and count show in CML?

A

WCC greatly increased, spectrum of myeloid cells, low Hb and high platelets

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28
Q

What are the likely findings of the bone marrow aspirate in CML?

A

HYPERCELLUAR aspirate

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29
Q

What do cytogenetics look for in CML?

A

The Ph(t(9;22)) mutation found in the blood and the bone marrow

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30
Q

What are the 2 key treatments fro CML?

A

Tyrosine Kinase inhibitors and Allogenic stem cell trasnplant

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31
Q

Name 3 tyrosine kinase inhibitors

A

Imatinib
Dasatinib
Nilotinib

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32
Q

What does ALL stand for?

A

Acute Lymphoblastic Leukaemia

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33
Q

Which age group does ALL affect?

A

Children under 6

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34
Q

What is the definition of ALL, ie what is the diagnostic criteria?

A

Lymphocytes more than 20% in the bone marrow

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35
Q

What percentage is in children in ALL?

A

75%

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36
Q

What is the incidence of ALL?

A

1-2/100’000

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37
Q

From what cell line do MOST of the ALL’s come from?

A

B cells

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38
Q

What are the KEY clinical symptoms of ALL?

A

Rapid bone marrow failure and increase in WCC causing:
Anaemia
Thrombocytopenia(purpura)
Infection owing to neutropenia

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39
Q

What are some other associated features of ALL?

A 
Night sweats
fever
Weight loss
Failure to thrive 
Bone pain 
Lymphadenopathy
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40
Q

What is a classical presentation fo a child with ALL?

A

A child with a new otherwise unexplained limp, or refusal to walk - always do a BLOOD FILM

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41
Q

What investigations are most appropriate for ALL?

A

Blood count and film and a bone marrow aspirate

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42
Q

What is the finding on blood flies and count in ALL?

A

Low RCV = Red Cell volume
Low Hb
Low or normal plateltes
V. raised WCC

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43
Q

What are the diagnostic findings on bone marrow aspirate in ALL?

A

> 20% lymphocytes in bone marrow aspirate

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44
Q

What other investigation might you do in ALL?

A

CSF examination

45
Q

What is the acute and emergency treatment for a child with ALL?

A

Steroids

46
Q

What is the long term management of a child with ALL?

A

Multi-agent chemotherapy to induce remission
Consolidation therapy
CNS directed treatment
Remission maintenance which low dose, long term ie 18 months of tablets/injections

47
Q

What is another option for ALL treatment? What is the risk?

A

Allogenic stem cll transplant = 10-30% risk mortality

48
Q

What are the risk factors for a poor prognosis is ALL?

A 
Over 30yo
Poor response to treatment 
High WCC
Immunophenotype (primate forms)
Cytogenetics
49
Q

What does CLL stand for?

A

Chronic Lymphocytic Leukaemia

50
Q

What is the epidemiology of CLL? Is it a common cancer?

A

Most common leukaemia 1700/yr

51
Q

What is the M:F ratio of CLL?

A

2:1

52
Q

Can this condition be familial?

A

Yes. occasionally

53
Q

How do people present with CLL?

A

Asymptomatic at presentation

54
Q

From what cell lines do CLL stem from?

A

B and T lymphocytes

55
Q

What are the common findings in clinical presentation in CLL?

A

Bone marrow failure: anaemia and thrombocytopenia
Lymphadenopathy
Splenomegaly
night sweats

56
Q

What are the less common findings in CLL?

A

Hepatomegaly
Infections
Weight Loss

57
Q

What is the diagnostic Criteria of CLL?

A

> 5x10^9 lymphocytes

Bone marrow: >30% lymphocytes

58
Q

What are the characteristic immunotyping features in CLL?

A

B cell markets CD 19. 20, 23 and CD5+

59
Q

What are the key investigations of CLL?

A

Blood film and count, bone marrow aspirate and immunotyping

60
Q

What are the associated findings in CLL?

A

Immune paresis( loss of Ig function) and haemolytic anaemia

61
Q

What percentage are DAGT positive in CLL?

A

20%

62
Q

What staging do we use for CLL?

A

BINET

63
Q

What is stage A CLL?

A

Less than 3 lymph nodes involved and no reduction on mortality compared to control

64
Q

What is stage B CLL?

A

More than 3 lymph nodes involved and a prognosis if 8 years

65
Q

What is stage C CLL?

A

Stage B + systemic symtoms = 6ys medican survival

66
Q

What is the management of CLL?

A 
Watchful waiting 
Cytotoxic Cehmotherapy
Monoclonal antibodies
Novel agents
Immunoglobulin infusions
67
Q

Give and example of a cytotoxic chemotherapy agent?

A

FLUDARABIN

68
Q

Give an example of a monoclonal antibody agent

A

RITUXIMAB

69
Q

Describe some novel agents for CLL?

A

Buton tyrosine kinase inhibitor e.g. IBRUTINIB
P13K inhibitor e.g. IDELASAB
BCL-2 inhibitor e.g. VENETOCLAX

70
Q

What are the indications for therapy in CLL?

A 
Progressive bone marrow failure 
Systemic symptoms
Lymphocyte count doubling in 6 months OR increase in 50% in 2 weeks 
Massive splenomegaly/ lymphadenopathy 
Autoimmune cytopenias
71
Q

What are the poor prognostics factors in CLL?

A 
advanced stage disease
Atypical lymphocyte morphology 
Rapid lymphocyte doubling
Loss/mutation p53; del 11q23 (ATM gene)
"Unmutated IgVH gene status
72
Q

When is HL most prevalent?

A

In a bimodal distribution so 15-20yo’s and then 70-85yo’d

73
Q

What is the M:F ratio in HL?

A

1.9:1

74
Q

What are the etiological factors of Hl?

A

Association of EBV, familial and geographical clustering

75
Q

Describe the histopathology of HL

A

1 Hodgkin cell sits in the lymph gland recruiting inflammatory cells into the environment to protect itself and then produces B symptoms

76
Q

What are the characteristic cells found in lymph node biopsy?

A

Reed-steinberg cells

77
Q

What is the classical presentation of HL?

A

Neck lymphadenopathy, which moves along the lymphatic chain
alcohol related lymph node pain
Hepatosplenomegaly

78
Q

What re the B symptoms of HL?

A 
Fever
Drenching night sweats
Weight loss >10% BW in 6 months 
Pruritus
Fatigue
79
Q

Is there bone marrow involvement in HL?

A

Yes

80
Q

What are the 4 investigation that you want to do for HL?

A

LYMPH NODE BIOPSY
CT scan
Bone marrow aspirate and
CXR for mediastinal involvement

81
Q

What are the 1st and 2nd stages of HL?

A

Ann Arbor System
1 = Lymphadenopathy on 1 side in 1 area
2 = unilateral lymphadenopathy in 2 areas

82
Q

What is the management of HL?

A

ABVD = combination chemotherapy of Adriamycin, Bleomycin, Vinblastine ad Dacarbazine +/- chemotherapy

83
Q

How do you monitor the response to treatment of HL?

A

PET scan to assess response and limit RT

84
Q

What are the 3rd and 4th stages of HL?

A

3= bilateral lymphadenopathy or spleen involvement

Stage 4 = above + liver, spleen or bone marrow involvement

85
Q

What does N-HL stand for?

A

Non-Hodgkin’s Lymphoma

86
Q

From what cell lineage does the NHL come from?

A 
80% = B lymphocytes
20% = T lymphocytes
87
Q

Is this a common type of lymphoma?

A

Yes the high grade type is the most common lymphoma

88
Q

What are the 2 grades of this disease?

A

High and low grade disease

89
Q

Describe the high grade features of NHL

A

Agressive and fast growing, needs combination chemotherapy and can be curable

90
Q

Describe the low grade features of NHL

A

This is indolent and asymptomatic, responds to chemo but is incurable, survival rates depend on the subtype

91
Q

What are the 2 most common histological types of lymphoma?

A 
Diffuse large B cell lymphoma(high grade)
Follicular lymphoma(low grade)
92
Q

What are common symptoms of NHL?

A

Lymphadenopathy
Hepatosplenomegaly
B symptoms
Bone marrow involvement

93
Q

Describe the 4 stages of NHL

A

1= 1 nodal group
2= 2 nodal groups on the same side of the diaphragm
3= nodal groups on both sides of the diaphragm +/- splenic involvement
4=disseminated involvement + one or more extra-lymphatic organ involvement

94
Q

How are you got going to diagnose NHL?

A

Lymph node biopsy
CT scan and
Bone marrow aspirate

95
Q

How do you monitor NHL?

A

With follow up PET CT’s

96
Q

What are the 2 strategies for management?

A

Low grade = watchful waiting

High grade = combination chemotherapy: anti-CD20 monoclonal antibody + chemo

97
Q

Do you get reed-steinberg cells in NHL?

A

NO!!!!! Thats the whole point

98
Q

What is multiple myeloma a cancer of?

A

The Plasma Cells

99
Q

What does the disorder produce? in MM

A

Damage to the plasma cells results in an unusually excessive production os a single immunoglobulin(paraprotein) ie either IgG or IgA

100
Q

What are the epidemiological factors in MM?

A

Peaks in the 7th decade

Commoner in the back population

101
Q

What are the 4 types of MM?

A

IgG = 55%
IgA = 21%
Light chain only = 22%
Other eg IgD/IgM = 2%

102
Q

What are the 2 big groups of effectors in MM?

A

Effects of plasma cell neoplasia

103
Q

What do the plasma cells cause in MM?

A

Effects os paraproteins

104
Q

What symptoms does Paraproteinaemia produce in MM?

A

Renal failure
Hyper-viscosity causing bleeding in the retinal, oral, nasal or cutaneous tissues
Cardiac failure
Hypogammaglobulinaema: impaired function of Ig

105
Q

What are the features of amyloidosis in MM?

A 
Nephrotic syndrome(check for paraprotiens)
Cardia failure
Carpal tunnel syndrome 
Autonomic neuropathy 
Cutanoeus infiltration
106
Q

What are the investigations for MM? + What is the diagnostic criteria

A

Bone marrow aspirate >10% os plasma cells in the bone marrow
If they have the presence of a paraprotein then diagnosed as MONOCLONAL GAMMOPATHY OF UNCERTAIN SIGNIFICANCE (MGUS) and no treatment required
+ CT head shows salt and pepper pot appearance of skill
+ Evidence of end organ damage

107
Q

What paraprotein tests can you do in MM?

A

Total immunoglobulin and the Ig subclasses
Serum protein electrophoresis
Immunofixation: IgG/ IgA parapotiens = myeloma note if IgM then lymphoma
Light chan examination

108
Q

What are the principles of management in MM?

A

Chemotherapy
Monoclonal antobodies
RT, steroids, autologous SC transplant
Biphosphonate therapy

109
Q

What symptoms do the plasma cells produce in MM?

A

Bone disease: lytic bone lesions, pathological fractures, cor compression and hypercalcaemia

Haematology Revision (8 decks)

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