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Leukaemia Flashcards

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1
Q

What are the main types of leukaemia?

A

Acute myeloid leukaemia
Acute lymphoblastic leukaemia
Chronic myeloid leukaemia
Chronic lymphoid leukaemia

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2
Q

What is the pathophysiology of ALL?

A

Arises from lymphoid progenitor cells that undergo malignant transformation

Most are B cell in origin
May arise from T cells

As clonal expansion occurs, these precursors replace other haematopoietic cells in the bone marrow

Classified as B cell lineage
T cell lineage

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3
Q

What cytogenic features are seen in ALL?

A

t(12;21) most common translocation seen in children - TEL-AML fusion gene

t(9;22) Philadelphia chromosome - BCR-ABL

t(4;11) in infants <12 months, rare in adults

Hyperdiploid karyotype
Hypodiploid karyotype

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4
Q

What are the clinical features of ALL?

A

Marrow suppression symptoms and lymphadenopathy

Marrow failure:
Anaemia - fatigue, SOB, angina
Neutropenia - recurrent infections
Thrombocytopenia - petechiae, nose bleeds, bruising

Tissue infiltration
Lymphadenopathy
Hepatosplenomegaly
Bone pain
Mediastinal mass - may result in SVCO
Testicular enlargement

Leucostasis
May occur due to large numbers of WCs entering blood stream
Organ dysfunction due to impairment through small vessels

Altered mental state, headache, SOB, visual changes

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5
Q

What is the presentation of T cell ALL?

A

Rarer than B cell form
Typically present in adolescent males
With lymphadenopathy or a mediastinal mass

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6
Q

What are the investigations for ALL?

A

Bloods
FBC, U&Es, LFTs, clotting
DDIMER, bone profile,
uric acid, LDH, BBV

Most will present with pancytopenia

Uric acid and LDH non specific markers of tumour border

DDIMER and coag for DIC

Imaging
CXR - mediastinal mass
CT chest, abdo pelvis for lympadenopathy and organ involvement
CT/MRI head exclude differentials, neurology

Bone marrow aspiration and biopsy, staining and review of cell morphology
Immunophenotyping

Blood smear
Pleural tap if pleural effusion
LP if CNS involvement

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7
Q

What are high-risk factors for adult patients, indicating a poorer prognosis?

A 
Age - worse with advancing age
Performance status > 1
WCC - >30 for B, >100 for T
Cytogenetics - 9;22, 4;11
Immunophenotype - proB, early and mature T
CNS involvement
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8
Q

What is the management of ALL?

A

Referral to haemato-oncology specialists

  1. Pre-phase therapy - steroids, with allopurinol and IV hydration, reduces risk of TLS

Can give rasburicase to prevent TLS as helps clears uric acid from body

Leucopheresis can help reduce WCC for TLS.
Anaemia and thrombocytopenia may need treatment, G-CSF for neutropenia.

  1. Induction chemotherapy
    For complete remission or molecular complete:
    Complete - not in bone marrow, peripheral blood or CSF
    MolecularCR - minimal disease not detectable by sensitive molecular probe
  2. Maintenance therapy
    Daily 6-mercaptopurine
    Weekly methotrexate
    Reduce risk of recurrence
  3. Stem cell transplant
    Allogenic
    Myeloablative transplant = high dose chemo, then stem cell transplant
  4. Palliative care
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9
Q

What complications are ALL patients at risk of?

A

TLS
Neutropenic sepsis
SVCO - dyspnoea, facial swelling, cough secondary to mediastinal mass
Chemo side effects - early mucositis, nausea, vomiting, hair loss or late - cardiomyopathy, secondary malignancies

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10
Q

What do you look for in a cytochemical stain in acute leukaemias?

A

TdT+ in lymphoblasts - ALL

Myeloperoxidase in myeloblasts - AML

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11
Q

How is philadelphia + ALL managed?

A

Stem cell transplant

Imatinib

TKI’s - tyrosine kinase inhibitors

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12
Q

What is APL? What genetics is it associated with?

A

Acute Promyelocytic Leukaemia

translocation of chromosome 15 and 17 t(15;17)

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13
Q

How does APL normally present? Describe the pathophysiology of this

A

Younger than AML and it’s other subtypes (age 25 ish)

build up of promyelocytes –> lots of Auer rods –> high coagulation risk –> DIC

Medical Emergency!

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14
Q

How is APL treated?

A

It responds to retinoic acid (ATRA)

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15
Q

What is myelodysplastic syndrome?
What would the bone marrow look like?
How would it present?

A

Condition which is a precursor of AML

Blasts build up in marrow but <20%

Same signs - cytopaenia, bruising etc.

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16
Q

Describe the age presentation of ALL vs AML

A

ALL is childhood (2-5)

AML is adults (65)

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17
Q

What are the blood results in ALL?

A

normocytic, normochromic anaemia
thrombocytopenia
leukocytosis but with neutropenia
reduced reticulocytes

Renal failure: raised K and phosphate

raised LDH

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18
Q

What is the bone marrow like in ALL?

A

hypercellular

blast cell infiltration

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19
Q

On cytochemical staining, what is seen in ALL? Compare this to AML?

A

blasts are TDT+ve

In AML it is myeloperoxidase +ve

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20
Q

What is ALL associated with?

A

Most common in children

Associated with Down’s

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21
Q

What is CLL associated with?

A

Most common leukaemia in adults overall
Associated with warm haemolytic anaemia
Richter’s transformation in lymphoma
Smudge/smear cells

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22
Q

What is CML associated with?

A

Has three phases
A 5 year - ‘asymptomatic chronic phase’
Associated with the Philadelphia chromosome

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23
Q

What is AML associated with?

A

Most common adult acute leukaemia
Can be the result of a transformation from a myeloproliferative disorder
Associated with Auer rods

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24
Q

What are the differentials for petechiae?

A 
Leukaemia
Meningococcal sepsis
Vasculitis
Henoch Schonlein Purpura
Idiopathic Thrombocytopenia Purpura 
Non accidental injury
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25
What is the pathogenesis of a haematological malignancy?
Cause - environment, toxin, virus infection, drug, genetic predisposition: translocation, deletion, duplication, point mutation Pathogenesis - altered gene expression, change in oncogene or tumour suppressor gene Leads to decrease in apoptosis and differentiation, and proliferation increase
26
What are lymphoid haematological malignancies?
Acute - lymphoblastic leukaemia ``` Chronic Lymphocytic leukaemia Non-Hodgkin lymphoma Hodgkin lymphoma Multiple myeloma ```
27
What are myeloid malignancies?
Acute myeloid leukaemia Chronic myeloid leukaemia Myelodysplasia Myeloproliferative disorders e.g. polycythaemia vera, essential thrombocytopenia, primary myelofibrosis
28
What would be shown on a blood film in T-ALL?
Bone marrow showing large number of lymphoblasts with a high nuclear/cytoplasmic ratio
29
What would be shown on a blood film in B-ALL?
Large blasts with characteristic vacuoles and blue cytoplasm
30
What are prognostic indicators in AML suggesting a better outcome?
Cytogenic changes - 8;21, 15;17, inversion 16 | Remission after one course of chemotherapy
31
What indicates poor risk in AML?
Cytogenic changes - monosomy 5, monosomy 7, complex charyotypes, 11q23 abnormalities Aged over 70
32
How can AML be classed?
Primary or secondary; as may follow a previous myeloproliferative or myelodysplastic event
33
What is the aetiology of AML?
Not completely understood Myelodysplastic syndrome and high risk features e.g. excessive blasts Congenital disorders e.g. Down's, Fanconi anaemia Radiation exposure Prev chemo Toxins - bezene, organochloride insecticides
34
What are the clinical features of AML?
Pancytopenia Fatigue, SOB, angina, recurrent infections, petechiae, nosebleeds Tissue infiltration Leucostasis
35
What are the investigations for AML?
Normocytic normochromic anaemia is common As is thrombocytopenia and reduced reticulocyte count Usual blood panel Clotting and DDIMER - DIC Bone profile, Mg Blood smear: Auer roads - azurophilic structures seen in myeloid blasts (also seen in myelodysplastic syndrome) Bone marrow aspirate Myeloid blast count of >20% LP if concern of CNS involvement
36
What is the management of AML?
Education and support Cytoreduction considered in signs of leukostasis and WBC count >100 with hydroxycarbamide Intrathecal chemo - cytarabine if CNS involved TLS - prophylaxis where indicated Chemo: Induction - cytarabine, daunorubicin and gemtuzumab Consolidation - IDAC Allogenic haematopoietic stem cell transplant following myeloablative conditioning regimes +- total body irradiation
37
What factors indicate poorer prognosis in AML?
'Secondary leukaemia' following a preceding haematological disorder e.g. MDS ``` Age >60 Poor performance status Multiple significant co-morbidities Prev haematological disorders, dysplasia Prev exposure to chemo/radio Certain disease subtypes ```
38
What are the phases of treatment for leukaemia?
First phase remission induction with high dose intensive combination chemo to re-establish normal haemopoiesis Then post induction chemo initially intensive Then for ALL less intensive maintenance chemo Requires 4-6 weeks in hospital
39
What is chronic lymphocytic leukaemia?
Lymphoproliferative disorder of B lymphocytes Results from abnormal clonal expansion of B cells Leads to widespread lymphadenopathy Due to genetic alterations and changes to the bone marrow microenvironment
40
What genetic alterations are associated with CLL?
``` TP53 mutation, major tumour suppressor gene 11q and 13q14 deletions Trisomy 12 Overexpression of BC12 proto-oncogene NOTCH1 mutation ```
41
What is monoclonal B cell lymphocytosis?
Premalignant disorder Genetic alterations allow the formation of a clone of B lymphocytes Overtime further mutations and bone marrow microenvironment changes allows progression to CLL
42
What are the clinical features of CLL?
Hallmark feature is lymphadenopathy due to infiltration of malignant B lymphocytes Large proportion may be asymptomatic so detected on routine blood tests or finding of abnormally enlarged but painless lymph nodes Weight loss, anorexia Fevers, night sweats Lethargy Lymphadenopathy, most commonly cervical, supraclavicular, axillary Hepatomegaly Splenomegaly
43
What features occur in association with complications of CLL?
Autoimmune haemolytic anaemia - pallor, SOB, weakness, dizziness Immune thrombocytopenia - petechiae, bruising, mucosal bleeding Hypogammaglobulinaemia - recurrent infections, organ specific
44
How can a diagnosis of CLL be made?
Excess lymphocytes found to be clonal (of same type) Assessed by flow cytometry Absolute B lymphocyte count of >5x10^9 for > 3 months or >1 cytopenia due to bone marrow infiltration And characteristic immunophenotype features and presence of disease manifestations
45
What is done for investigations for CLL?
Clinical examination to determine presence or absence of lymph node involvement inc specific sites, splenomegaly and hepatomegaly Bloods - FBC, routine biochemistry, blood film, haemolysis screen, immunoglobulins Cytogenetics and immunophenotyping Blood film Lymphocytes, smudge cells Bone marrow assessment not usually required unless alternative diagnosis CT imaging if concerned about lymphomatous transformation CXR Lymph node biopsy Virology
46
What is the staging of CLL?
Binet Staging Based on number of lymphoid sites affected on clinical examination Stage A < 3 sites Stage B >3 lymphoid sites Stage C - presence of anaemia or thrombocytopenia An area is counted as one regardless of whether unilateral or bilateral Rai Staging Based on expected natural progression to marrow failure Stage 0 - lymphocytosis Stage I-II lymphocytosis, lymphadenopathy, organomegaly Stage III-IV lymphocytosis, anaemia, thrombocytopenia, lymphadenopathy, organomegaly
47
What are some prognostic factors for CLL?
Lymphocyte doubling time Genetic abnormalities e.g. TP53, trisomy 12 Beta 2 microglobulin Mutated immunoglobulin heavy chain variable genes
48
What is the management for CLL?
Watch and wait if asymptomatic indolent Assessment and FBC at 3 monthly intervals Front line therapy with no TP53 mutations - Fludarabine, cyclophosphamide, Rituximab Front line therapy with mutations Ibrutinib, Rituximab Chemo - e.g. chlorambucil Small molecule inhibitors e.g. venetoclax, Ibrutinib Monoclonal antibodies e.g. Rituximab Corticosteroids Allogenic stem cell transplantation Supportive care - vaccination, abx, intravenous immunoglobulins, PJP and herpes zoster prophylaxis
49
What is Richter transformation?
CLL becomes a form of aggressive lymphoma | Associated with rapid deterioration
50
What are some of the complications of CLL?
May transform into another lymphoproliferative disorder Prolymphocytic leukaemia Hodgkin lymphoma Multiple myeloma Secondary infections - herpes, PJP, bacterial Autoimmune complications Hyperviscosity syndrome Secondary malignancies
51
What are the indications for treatment of CLL?
Bone marrow failure - Hb <100, plts <100 x 10^9 g/L Massive, progressive or symptomatic splenomegaly Massive progressive or symptomatic lymphadenopathy Progressive lymphocytosis Autoimmune complications not responsive to steroids Symptomatic/functional extra nodal sites Disease related symptoms
52
What disease related symptoms should you be on the look out for, for CLL?
Significant weight loss Severe fatigue >2 weeks of fever >1 month of night sweats, without infection
53
What is chronic myeloid leukaemia associated with?
Philadelphia chromosome - translocation of 9 and 22 | Results in a constitutively activated tyrosine kinase
54
What are the clinical features of CML?
Some asymptomatic, or non vague features, picked up on other tests Fatigue, weight loss Night sweats, anaemia SOB, angina Thrombocytopenia - petechiae, nose bleeds, bruising Splenomegaly - early satiety, abdominal pain Bone pain Leucostasis - headache, breathlessness, visual changes, priapism Splenomegaly Hepatomegaly Lymphadenopathy Leucostasis - altered mental state, priapism
55
What are the investigations for CML?
Bloods - excessive granulocytosis with typical left shift Bloods FBC - raised WCC Blood film - immature and mature myeloid cells LDH, urate and potassium useful markers of disease Renal function, LFTs, bone profile, Mg, lipids, HbA1c Cytogenetics, FISH to identify Ph chromosome - BCR-ABL1 fusion Bone marrow aspirate Marrow is hyper cellular with myeloid hyperplasia
56
Why is allopurinol given in chemo treatments?
Reduce level of uric acid and risk of tumour lysis syndrome
57
What are the disease phases of CML?
``` 1. Chronic phase Most present at this point Features non-specific Fatigue, weight loss, NSs Prior to advance tx, this phase would last 3-5 years ``` 2. Accelerated phase Features more apparent and severe, harder to treat Lasts 6-18 months untreated Blasts in blood or marrow15-29%, basophils in blood Persistent thrombocytopenia Clonal chromosome abnormalities in Ph cells ``` 3. Blast crisis Resembles an acute leukaemia Without tx, survival is a few months Blasts in blood or bone marrow >30% Extramedullary blast proliferation ```
58
What is the management of CML?
Tyrosine kinase inhibitors - block the enzyme created by BCR-ABL1 fusion gene Invasive chemo reserved for patients with plastic transformation Allogenic stem cell transplant for chronic patients
59
What tyrosine kinase inhibitors are used in the treatment of CML?
Imatinib Dasatinib Nilotinib
60
What are some side effects of tyrosine kinase inhibitors used in CML?
``` Nausea, vomiting Oedema, cramps, rashes GI symptoms, headache Fatigue Derangement of LFTs Pleuro-pulmonary toxicity ```
61
What are the phases of CML?
Chronic phase May need emergency cytoreduction if WCC v high Good oral hydration and allopurinol to reduce risk of TLS, use of TKIs Advanced phase May have undergone blastic transformation Second generation TKI with or without intensive chemo
62
What are the complications of CML?
Thrombotic event | Blast transformation to an acute leukaemia
63
What cytogenetic findings suggest CML?
Philadelphia!! Seen in 95% of patients with CML
64
What is seen on a blood film of CML? and what is seen in the bone marrow?
Granulocytes at all different stages of development BM: hypercellular with ++ granulocytes
65
Blood results seen in CML?
+++ leukocytosis normocytic, normochromic anaemia Thrombocytosis progresses to penia
66
What is Richter transformation? What is the pathophysiology? How does it present?
Transformation of CLL to a high grade lymphoma Due to leukaemia cells infiltrating the lymph node SUDDEN deterioration of symptoms - B symptoms - lymph node swelling - abdo pain and nausea
67
What is hypogammaglobulinaemia and what does it lead to?
It results in a lack of antibodies and therefore infections
68
What is seen on a blood film in CLL?
Smudge/smear cells Lymphocytosis NOT blasts
69
Poor prognostic features of AML?
>60 >20% blasts after first chemo chromosome deletions
70
Characteristics of the bone marrow in AML?
Hypercellular | >20% Blast cells
71
What is seen on the blood film of AML?
Blast cells with Auer rods
72
What is myelodysplastic syndrome? What would the bone marrow look like? How would it present?
Condition which is a precursor of AML Blasts build up in marrow but <20% Same signs - cytopaenia, bruising etc.
73
When are most CML's diagnosed?
in the chronic phase - incidentally found on routine bloods
74
What is a blast crisis?
No ability to differentiate so resemble acute leukaemia Bone marrow exhaustion and large tumour burden - systemically unwell and rapidly fatal
75
What is regularly monitored throughout management of CML?
FISH studies - show % bone marrow cells Ph+

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