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

3 Big: Leukaemias, Lymphomas and Myelomas Flashcards

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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
What does hyperleukostasis cause?
Fundal haemorrhage Venous congestion Altered consciousness Respiratory failure
26
What investigations are key if you suspect CML?
Blood count and blood film | Bone marrow aspirate
27
What will the blood film and count show in CML?
WCC greatly increased, spectrum of myeloid cells, low Hb and high platelets
28
What are the likely findings of the bone marrow aspirate in CML?
HYPERCELLUAR aspirate
29
What do cytogenetics look for in CML?
The Ph(t(9;22)) mutation found in the blood and the bone marrow
30
What are the 2 key treatments fro CML?
Tyrosine Kinase inhibitors and Allogenic stem cell trasnplant
31
Name 3 tyrosine kinase inhibitors
Imatinib Dasatinib Nilotinib
32
What does ALL stand for?
Acute Lymphoblastic Leukaemia
33
Which age group does ALL affect?
Children under 6
34
What is the definition of ALL, ie what is the diagnostic criteria?
Lymphocytes more than 20% in the bone marrow
35
What percentage is in children in ALL?
75%
36
What is the incidence of ALL?
1-2/100'000
37
From what cell line do MOST of the ALL's come from?
B cells
38
What are the KEY clinical symptoms of ALL?
Rapid bone marrow failure and increase in WCC causing: Anaemia Thrombocytopenia(purpura) Infection owing to neutropenia
39
What are some other associated features of ALL?
``` Night sweats fever Weight loss Failure to thrive Bone pain Lymphadenopathy ```
40
What is a classical presentation fo a child with ALL?
A child with a new otherwise unexplained limp, or refusal to walk - always do a BLOOD FILM
41
What investigations are most appropriate for ALL?
Blood count and film and a bone marrow aspirate
42
What is the finding on blood flies and count in ALL?
Low RCV = Red Cell volume Low Hb Low or normal plateltes V. raised WCC
43
What are the diagnostic findings on bone marrow aspirate in ALL?
>20% lymphocytes in bone marrow aspirate
44
What other investigation might you do in ALL?
CSF examination
45
What is the acute and emergency treatment for a child with ALL?
Steroids
46
What is the long term management of a child with ALL?
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
What is another option for ALL treatment? What is the risk?
Allogenic stem cll transplant = 10-30% risk mortality
48
What are the risk factors for a poor prognosis is ALL?
``` Over 30yo Poor response to treatment High WCC Immunophenotype (primate forms) Cytogenetics ```
49
What does CLL stand for?
Chronic Lymphocytic Leukaemia
50
What is the epidemiology of CLL? Is it a common cancer?
Most common leukaemia 1700/yr
51
What is the M:F ratio of CLL?
2:1
52
Can this condition be familial?
Yes. occasionally
53
How do people present with CLL?
Asymptomatic at presentation
54
From what cell lines do CLL stem from?
B and T lymphocytes
55
What are the common findings in clinical presentation in CLL?
Bone marrow failure: anaemia and thrombocytopenia Lymphadenopathy Splenomegaly night sweats
56
What are the less common findings in CLL?
Hepatomegaly Infections Weight Loss
57
What is the diagnostic Criteria of CLL?
>5x10^9 lymphocytes | Bone marrow: >30% lymphocytes
58
What are the characteristic immunotyping features in CLL?
B cell markets CD 19. 20, 23 and CD5+
59
What are the key investigations of CLL?
Blood film and count, bone marrow aspirate and immunotyping
60
What are the associated findings in CLL?
Immune paresis( loss of Ig function) and haemolytic anaemia
61
What percentage are DAGT positive in CLL?
20%
62
What staging do we use for CLL?
BINET
63
What is stage A CLL?
Less than 3 lymph nodes involved and no reduction on mortality compared to control
64
What is stage B CLL?
More than 3 lymph nodes involved and a prognosis if 8 years
65
What is stage C CLL?
Stage B + systemic symtoms = 6ys medican survival
66
What is the management of CLL?
``` Watchful waiting Cytotoxic Cehmotherapy Monoclonal antibodies Novel agents Immunoglobulin infusions ```
67
Give and example of a cytotoxic chemotherapy agent?
FLUDARABIN
68
Give an example of a monoclonal antibody agent
RITUXIMAB
69
Describe some novel agents for CLL?
Buton tyrosine kinase inhibitor e.g. IBRUTINIB P13K inhibitor e.g. IDELASAB BCL-2 inhibitor e.g. VENETOCLAX
70
What are the indications for therapy in CLL?
``` 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
What are the poor prognostics factors in CLL?
``` advanced stage disease Atypical lymphocyte morphology Rapid lymphocyte doubling Loss/mutation p53; del 11q23 (ATM gene) "Unmutated IgVH gene status ```
72
When is HL most prevalent?
In a bimodal distribution so 15-20yo's and then 70-85yo'd
73
What is the M:F ratio in HL?
1.9:1
74
What are the etiological factors of Hl?
Association of EBV, familial and geographical clustering
75
Describe the histopathology of HL
1 Hodgkin cell sits in the lymph gland recruiting inflammatory cells into the environment to protect itself and then produces B symptoms
76
What are the characteristic cells found in lymph node biopsy?
Reed-steinberg cells
77
What is the classical presentation of HL?
Neck lymphadenopathy, which moves along the lymphatic chain alcohol related lymph node pain Hepatosplenomegaly
78
What re the B symptoms of HL?
``` Fever Drenching night sweats Weight loss >10% BW in 6 months Pruritus Fatigue ```
79
Is there bone marrow involvement in HL?
Yes
80
What are the 4 investigation that you want to do for HL?
LYMPH NODE BIOPSY CT scan Bone marrow aspirate and CXR for mediastinal involvement
81
What are the 1st and 2nd stages of HL?
Ann Arbor System 1 = Lymphadenopathy on 1 side in 1 area 2 = unilateral lymphadenopathy in 2 areas
82
What is the management of HL?
ABVD = combination chemotherapy of Adriamycin, Bleomycin, Vinblastine ad Dacarbazine +/- chemotherapy
83
How do you monitor the response to treatment of HL?
PET scan to assess response and limit RT
84
What are the 3rd and 4th stages of HL?
3= bilateral lymphadenopathy or spleen involvement | Stage 4 = above + liver, spleen or bone marrow involvement
85
What does N-HL stand for?
Non-Hodgkin's Lymphoma
86
From what cell lineage does the NHL come from?
``` 80% = B lymphocytes 20% = T lymphocytes ```
87
Is this a common type of lymphoma?
Yes the high grade type is the most common lymphoma
88
What are the 2 grades of this disease?
High and low grade disease
89
Describe the high grade features of NHL
Agressive and fast growing, needs combination chemotherapy and can be curable
90
Describe the low grade features of NHL
This is indolent and asymptomatic, responds to chemo but is incurable, survival rates depend on the subtype
91
What are the 2 most common histological types of lymphoma?
``` Diffuse large B cell lymphoma(high grade) Follicular lymphoma(low grade) ```
92
What are common symptoms of NHL?
Lymphadenopathy Hepatosplenomegaly B symptoms Bone marrow involvement
93
Describe the 4 stages of NHL
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
How are you got going to diagnose NHL?
Lymph node biopsy CT scan and Bone marrow aspirate
95
How do you monitor NHL?
With follow up PET CT's
96
What are the 2 strategies for management?
Low grade = watchful waiting | High grade = combination chemotherapy: anti-CD20 monoclonal antibody + chemo
97
Do you get reed-steinberg cells in NHL?
NO!!!!! Thats the whole point
98
What is multiple myeloma a cancer of?
The Plasma Cells
99
What does the disorder produce? in MM
Damage to the plasma cells results in an unusually excessive production os a single immunoglobulin(paraprotein) ie either IgG or IgA
100
What are the epidemiological factors in MM?
Peaks in the 7th decade | Commoner in the back population
101
What are the 4 types of MM?
IgG = 55% IgA = 21% Light chain only = 22% Other eg IgD/IgM = 2%
102
What are the 2 big groups of effectors in MM?
Effects of plasma cell neoplasia
103
What do the plasma cells cause in MM?
Effects os paraproteins
104
What symptoms does Paraproteinaemia produce in MM?
Renal failure Hyper-viscosity causing bleeding in the retinal, oral, nasal or cutaneous tissues Cardiac failure Hypogammaglobulinaema: impaired function of Ig
105
What are the features of amyloidosis in MM?
``` Nephrotic syndrome(check for paraprotiens) Cardia failure Carpal tunnel syndrome Autonomic neuropathy Cutanoeus infiltration ```
106
What are the investigations for MM? + What is the diagnostic criteria
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
What paraprotein tests can you do in MM?
Total immunoglobulin and the Ig subclasses Serum protein electrophoresis Immunofixation: IgG/ IgA parapotiens = myeloma note if IgM then lymphoma Light chan examination
108
What are the principles of management in MM?
Chemotherapy Monoclonal antobodies RT, steroids, autologous SC transplant Biphosphonate therapy
109
What symptoms do the plasma cells produce in MM?
Bone disease: lytic bone lesions, pathological fractures, cor compression and hypercalcaemia

Haematology Revision (8 decks)

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