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Y4 Cancer Care > 13 - Haematological 2 > Flashcards

13 - Haematological 2 Flashcards

1
Q

What is leukaemia and what is the difference between acute and chronic leukaemia?

A
  • Leukaemia are a group of malignancies that arise in the bone marrow that cause excessive amount of one type of WBC
  • Classified as acute or chronic and by the lineage of stem cells they affect (myeloid or lymphoid)
  • Acute is due to impaired cell differentiation, so large numbers of malignant precursor cells in the bone marrow; on the other hand, chronic leukaemia is the result of excessive proliferation of mature malignant cells, but cell differentiation is unaffected
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2
Q

Why does leukaemia lead to a pancytopenia?

A

Excessive production of a single type of cell can lead to suppression of the other cell lines

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3
Q

What ages do each of the types of leukaemia tend to affect?

A

“ALL CeLLmates have CoMmon AMbitions”

45-75 in steps of 10 years

  • Under 5 and over 45 – acute lymphoblastic leukaemia (ALL)
  • Over 55 – chronic lymphocytic leukaemia (CeLLmates)
  • Over 65 – chronic myeloid leukaemia (CoMmon)
  • Over 75 – acute myeloid leukaemia (AMbitions)
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4
Q

Leucostasis may occur in leukaemia due to the increased number of white cells in the blood. How may this present?

A
  • Altered mental state
  • Headache
  • Breathlessness
  • Visual changes
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5
Q

When a bone marrow aspirate/biopsy is done, what are they sent off for?

A
  • Staining (Wright or Giemsa) to look at cell morphology
  • Cytogenetics
  • Immunophenotyping for cell lineage
  • Flow cytometry
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6
Q

What is the most common leukaemia in adults?

(image really important)

A

CLL!!!!!

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7
Q

What is the epidemiology and aetiology/risk factors of AML?

A

Epidemiology

  • More common in men and diagnosis age 70

Aetiology

  • Myelodysplastic syndrome: increased risk
  • Down’s syndrome
  • Congenital neutropaenia
  • Fanconi anaemia
  • Radiation exposure
  • Previous administration of chemotherapy
  • Toxins: benzene and organochlorine insecticides
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8
Q

How does leukaemia present?

A

Marrow failure

  • Anaemia: fatigue, breathlessness, angina
  • Neutropenia: recurrent infections
  • Thrombocytopenia: petechiae, nose bleeds, bruising

Tissue infiltration

  • Lymphadenopathy
  • Hepatosplenomegaly: early satiety and reduced appetite
  • Bone pain
  • Gum hypertrophy
  • Violaceous skin deposits
  • Testicular enlargement
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9
Q

What investigations are done if you suspect a patient to have leukaemia, how urgently do you do this and what features would warrant this referral

A

48 hours FBC

  • Bleeding, bruising or petechiae
  • Bone pain
  • Persistent unexplained fatigue
  • Unexplained fever
  • Hepatosplenomegaly
  • Persistent recurrent infections
  • Unexplained lymphadenopathy
  • Pallor
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10
Q

What will be seen on a FBC if there is leukaemia?

A
  • Normocytic normochromic anaemia
  • Reduced reticulocyte count
  • Thrombocytopenia
  • Raised white cell count
  • Circulating myeloblasts
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11
Q

What further investigations should be ordered for leukaemia?

A

Bloods

  • FBC
  • U+Es
  • LFTs
  • Clotting screen: for baseline and to look for DIC
  • DDIMER
  • Bone profile & Mg
  • Uric acid
  • LDH
  • Blood borne virus screen
  • Blood smear should be completed in all patient!!!!

Bone marrow aspirate and biopsy

For a definitive diagnosis

Imaging

  • CT CAP for staging
  • CXR for mediastinal mass

Lumbar puncture

If there is concern of CNS involvement

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12
Q

What is LDH a marker of?

A

Increased cell turnover

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13
Q

What is seen on blood film with AML?

A

Auer rods - Azurophilic structures seen in myeloid blasts

Also seen in myelodysplastic syndrome

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14
Q

What is diagnostic of AML on bone marrow aspirate/biopsy?

A

Myeloid blast count of > 20% (of 500 bone marrow cells).

Aspirate and biopsy samples are used for cytogenetics, immunophenotyping and flow cytometry

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15
Q

How is AML managed?

A

Initial management

Managed in specialist centres and offered any clinical trials if suitable

  • Education and support: coordinated by designated nurse
  • Supportive care: monitored for infections and coagulopathy
  • Cytoreduction
  • CNS involvement: started on intrathecal chemotherapy (cytarabine)
  • Tumour lysis syndrome: Should be anticipated, prophylaxis should be given

Chemotherapy or Haematopoietic stem cell transplantation

  • Induction and consolidation (and occasionally maintenance) stages
  • Allogenic stem cell transplant
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16
Q

When is cytoreduction done and how?

A

Patients with signs of leukostasis and WBC > 100 × 109/L

Hydroxycarbamide

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17
Q

How does an allogenic stem cell transplant work for AML?

A

Given myeloablative conditioning regimes (+/- total body irradiation) aimed at eliminating disease and allowing for a graft (the allo HCT) versus leukaemia reaction.

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18
Q

What are some poor prognostic indicators in AML?

A
  • Age (> 60)
  • Poor performance status
  • Multiple significant co-morbidities
  • Previous haematological disorders / dysplasia
  • Previous exposure to chemo/radio-therapy
  • Certain disease subtypes
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19
Q

What is the prognosis with AML if left untreated?

A

2 months

If treated 20% 5 year survival

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20
Q

How common are leukaemias?

A

12th most common cancer in the UK

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21
Q

What is the epidemiology of ALL and aetiology/risk factors?

A

Mostly affects under 4s

Genetics and Environment (e.g viruses)

Common in Downs syndrome

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22
Q

What are the most common presenting symptoms of ALL?

A
  • Bone pain
  • Lymphadenopathy
  • Symptoms of pancytopenia
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23
Q

What are some genetic mutations in ALL?

A

Philadelphia chromosome t(9:22)

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24
Q

What are the different subtypes of ALL and what is the most common?

A
  • Common ALL (75%): CD10 present, pre-B phenotype
  • T-cell ALL (20%): usually in adolescent males with mediastinal mass
  • B-cell ALL (5%)

B cell is most common!!!!!!!!

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25
Q

What do you see on a blood smear with ALL?

A

Blast cells

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26
Q

What are poor prognostic factors with ALL?

A

Typical cure rate 70 to 90%

  • Age (<2 or >10)
  • Male
  • Non-caucasian
  • Performance status > 1
  • White cell count > 20 at diagnosis
  • Cytogenetics
    • t(9;22) - Philadelphia chromosome
    • t(4;11)
  • CNS involvement
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27
Q

How is ALL managed?

A

Chemotherapy +/- Bone Marrow transplant

  • Refer to specialist centre and enrol in clinical trials

Pre-phase and supportive therapy

  • Pre-phase therapy: commenced on steroids with allopurinol and IV hydration to reduce risk of TLS
  • Leucopheresis: helps to mitigate the risk of TLS.
  • Supportive therapy: anaemia and thrombocytopenia may require treatment if severe. G-CSF may be given.

Induction chemotherapy

Those with CNS disease require intrathecal chemotherapy and prophylactic therapy may be used in those without to reduce the risk of CNS relapse

Maintenance therapy

Daily 6-mercaptopurine and weekly methotrexate

Stem cell transplant

Allogeneic stem-cell transplant may be considered. Reduces risk of relapse

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28
Q

What are some of the complications of ALL?

A
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29
Q

What is the characteristic pathophysiology of CML?

A

Philadelphia (Ph) chromosome

An abnormal chromosome 22 (t 9:22) that results in a constitutively activated tyrosine kinase

BCR-ABL protooncogene

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30
Q

How does CML tend to present?

A
  • In 50s and 60s with non-specific symptoms like fatigue, fever, night sweats
  • Lots are diagnosed incidentally by FBC showing raised WBC in all cell lines
  • Often have splenomegaly
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31
Q

How is CML definitively diagnosed?

A

Bone marrow biopsy/aspirate: allows review of percentages of blasts, promyelocytes, basophils and other haematological cell types for staging of phase as well as material for cytogenetics. Proportion of blasts and basophils help to categorise the phase of disease.

Marrow tends to be hypercellular with myeloid hyperplasia in chronic phase

Cytogenetic or FISH: find Philadelphia chromosome

Blood film: Immature and mature myeloid cells all at different stages of maturation

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32
Q

What white cell is a prognostic marker for CML?

A

Basophil

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33
Q

What are some baseline investigations you should do with CML?

A
34
Q

What are the three stages of CML, how do they present and how long do they last for?

A

1. Chronic phase

> 85%) present in the chronic phase. Clinical features non-specific e.g fatigue, weight loss and night sweats. Without treatment lasts 3-5 years

2. Accelerated phase

Features more apparent and severe and more difficult to treat and outcomes worse. Untreated this phase lasts around 6-18 months.

3. Blast crisis

Resembles an acute leukaemia with the rapid expansion of blasts. Without treatment survival is typically a few months. It is defined by ELN as:

35
Q

How can you tell the difference between the accelerated phase and blast crisis in CML?

A

Accelerated:

  • Blasts in blood or marrow 15–29%, or blasts plus promyelocytes in blood or marrow >30%, with blasts <30%
  • Basophils in blood ≥20%

Blast Crisis:

  • Blasts in blood or marrow ≥30%
  • Extramedullary blast proliferation, apart from spleen
36
Q

How is CML treated?

A

IT S CURABLE

  • First-line: Tyrosine kinase inhibitor, good response in chronic phase
  • Chemotherapy: Hydroxyurea or Interferon-alpha
  • Allogenic bone marrow transplant
37
Q

Give some examples of Tyrosine Kinase inhibitors used in CML and the side effects of these?

A
  • Imatinib: Side effects include nausea & vomiting, oedema, cramps, rashes, GI symptoms, headache and fatigue
  • Dasatinib: Can cause pleuro-pulmonary toxicity
  • Nilotinib: Side effects include cytopenias, headache, nausea, change in bowel habit, rash, pruritus, fatigue and derangement of LFTs. May cause prolonged QT
38
Q

How is CML management different between chronic and advance phase?

A

Chronic phase

  • Emergency cytoreduction with very elevated WCC at diagnosis (e.g. > 100 ×109/L)
  • Good oral hydration and allopurinol to reduce risk of TLS
  • TKIs
  • Allogenic SCT if failed initial TKI therapy

Advanced phase

  • All patients should be treated as part of a clinical trial
  • Second generation TKI with or without intensive chemotherapy
  • Allo-SCT offers potential cure in appropriate patients
39
Q

What is the prognosis with CML?

A
  • If newly diagnosed chronic phase CML have a near normal life-expectancy
  • Ages of 15-64: 90% 5-year survival
  • 65 and older: 40% 5-year survival
40
Q

CLL is the most common leukaemia in adults over 55. What is the aetiology and pathophysiology of this?

A

Chronic proliferation of a single type of well differentiated lymphocyte, usually B-lymphocytes

Genetic alterations

  • TP53 mutation: major tumour suppressor gene, linked to a poor response to treatment.
  • 11q and 13q14 deletions
  • Trisomy 12: presence of an extra 12th chromosome
  • Overexpression of BCL2 proto-oncogene
  • NOTCH1 mutation
41
Q

What is the natural disease history of CLL?

A

RELAPSING AND REMITTING

Initial event or abnormal reaction to an antigen leads to genetic alterations that allow the formation of a clone of B lymphocytes. This is a premalignant disorder, monoclonal B cell lymphocytosis (MBL)

Overtime, further genetic mutations and bone marrow microenvironment changes promote the progression to CLL. This transformation from MBL to CLL occurs at a rate of 1% per year

May remain asymptomatic for many years. The symptomatic stage of CLL is characterised by progressive lymphadenopathy, which includes splenomegaly and hepatomegaly, that occurs due to the accumulation of incompetent lymphocytes.

42
Q

How does CLL present?

A
  • Lymphadenopathy: hallmark feature due to infiltration of malignant B-lymphocytes
  • Asymptomatic: detected on routine blood tests
  • Recurrent infections: due to low IgG
43
Q

What investigations are done to diagnose CLL? (different to other leukaemias)?

A

DO NOT NEED BONE MARROW ASSESSMENT

  • FBC: persistent lymphocytosis and normocytic anaemia
  • Cytogenetics and Immunophenotyping: done by flow cytometry, proves lymphocytes are clonal. Can also look for mutations like TP53
  • Blood film: smear or ‘smudge’ cells. These are artefacts due to damaged lymphocytes
44
Q

What are some further investigations you should do with a diagnosis of CLL and why?

A
  • Routine biochemistry: U&E, bone profile, LFTs
  • Haemolysis screen (at risk of AIHA): Direct antiglobulin test (DAT), haptoglobin, LDH, unconjugated bilirubin, reticulocytes
  • Immunoglobulins: at risk of secondary hypogammglobulinaemia
  • CXR: look for pulmonary lymphadenopathy.
  • Lymph node biopsy: if concern about lymphomatous transformation.
  • Virology: important prior to initiation of treatment. Hepatitis B, hepatitis C, HIV,CMV
45
Q

How is CLL staged?

A

Binet or Rai

Binet staging

Lymphoid sites are cervical nodes, axillary nodes, inguinal nodes, spleen, and liver

  • Stage A: <3 lymphoid sites
  • Stage B: ≥3 lymphoid sites
  • Stage C: presence of anaemia (<100 g/L) and/or thrombocytopaenia (<100 x10^9/L)

Rai staging

Based on natural progression of CLL

  • Stage 0 (lymphocytosis): 25% at initial diagnosis
  • Stage I-II (lymphocytosis + lymphadenopathy + organomegaly): 50% at initial diagnosis
  • Stage III-IV (lymphocytosis + anaemia or thrombocytopaenia +/- lymphadenopathy/ organomegaly): 25% at initial diagnosis
46
Q

What are some prognostic indicator in CLL?

A
  • Binet and Rai stage
  • Lymphocyte doubling time
  • Genetic abnormalities on cytogenetics: TP53, del(11q), trisomy 12, and del(13q)
  • Beta-2-microglobulin: correlates with disease stage and tumour burden
47
Q

If patients with CLL are asymptomatic how are they treated?

A

Watch and wait

If asymptomatic, indolent disease without poor prognostic factors and Binet stage A/B or Rai stage <3

Full blood count at 3 monthly intervals

At 12 months, treatment decisions can be decided based on the trajectory of the condition or develop of active/symptomatic disease

48
Q

What are indications for treatment with CLL?

A

Need active disease. Need one of iwCLL criteria:

  • Bone marrow failure (Hb < 100 g/L, plts <100 x10^9/L)
  • Massive, progressive or symptomatic splenomegaly (≥6 cm)
  • Massive, progressive or symptomatic lymphadenopathy (≥10 cm)
  • Progressive lymphocytosis (≥50% over 2 months or doubling time < 6 months)
  • Autoimmune complications not responsive to steroids (e.g. ITP/AIHA)
  • Symptomatic/functional extranodal sites (e.g. skin, kidney, lung, spine)
  • Disease-related symptoms (e.g. significant weight loss, severe fatigue, >2 weeks of fever or ≥1 month of night sweats without infection)
49
Q

What does treatment depend on in CLL?

A
  • Patient fitness and performance status
  • Co-morbidities
  • Mutational analysis (e.g. TP53 mutations)
  • First-line treatment or treating relapse/refractory disease
50
Q

How is active CLL treated medically/surgically?

A

Pharmacotherapy

  • Chemotherapy
    • Chlorambucil: cross-links DNA leading to damage and apoptosis.
    • Fludarabine: purine analog that inhibits DNA synthesis
    • Bendamustine: alkylating agent that cross-links DNA
  • Small molecule inhibitors
    • Ibrutinib: tyrosine kinase inhibitor. TP53 mutations
    • Idelalisib: phosphoinositide 3-kinase inhibitor.
    • Venetoclax: BCL2 inhibitor
  • Monoclonal antibodies
    • Rituximab/Obinutuzumab/Ofatumumab: Anti-CD20 antibodies that target B lymphocytes
  • Other
    • Corticosteroids: in extremely frail patients or to treat autoimmune complications including haemolytic anaemia and immune thrombocytopaenia

Allogenic stem cell transplantation

  • If fail chemotherapy and BCR inhibitor therapy
  • TP53 mutations that do not respond to treatment or relapse
  • Richter’s transformation
51
Q

What supportive care is done in CLL?

A
  • Vaccination: influenza, pneumococcal
  • Antibiotics for infections
  • Consider IVIG: treatment of secondary hypogammaglobulinaemia (i.e. IgG < 5g/L)
  • Consider (PJP) and herpes zoster prophylaxis: in patients on treatment for relapsed CLL
52
Q

What autoimmune complications are patients with CLL at risk of?

A
  • AIHA
  • ITP
53
Q

What are some of the complications of CLL?

A

Histological transformation

  • Richter transformation: aggressive lymphoma, 5-8 month survival
  • Prolymphocytic leukemia
  • Hodgkin lymphoma
  • Multiple myeloma

Other complications

  • Secondary infections: herpes zoster, PJP, bacterial infections
  • Autoimmune complications: AIHA, immune thrombocytopaenia
  • Hyperviscosity syndrome
  • Secondary malignancies
54
Q

How may you know that Richter’s transformation has happened in CLL?

A

Ritcher’s transformation occurs when leukaemia cells enter the lymph node and change into a high-grade, fast-growing non-Hodgkin’s lymphoma

Ritcher’s transformation is indicated by one of the following symptoms:

  • lymph node swelling
  • fever without infection
  • weight loss
  • night sweats
  • nausea
  • abdominal pain
55
Q

What is the prognosis with CLL?

A

1/3 of cases don’t progress, 1/3 of cases progress slowly, and 1/3 of cases progress actively

56
Q

Why is ESR massively elevated in myeloma?

A

Increase in proteins within the plasma, either due to an abnormal protein such as a paraprotein in myeloma, or a polyclonal increase in proteins secondary to some other underlying inflammatory pathology

57
Q

When is Rasburicase given over Allopurinol?

A

When patients are high risk for TLS e.g haematological malignancy

58
Q

What are myeloproliferative disorders and what are the three main ones?

A

Uncontrolled proliferation of a single type of stem cell, type of bone marrow cancer

  • Primary myelofibrosis
  • Polycythaemia vera
  • Essential thrombocythaemia
59
Q

What gene mutations are associated with myeloproliferative disorders and what is the risk with these disorders?

A

Risk of transformation to AML

  • JAK2
  • MPL
  • CALR
60
Q

What is myelofibrosis?

A

Can be result of primary myelofibrosis, polycythaemia vera or essential thrombocythaemia

Proliferation of the cell line leads to fibrosis of the bone marrow due to cytokines that are released from the proliferating cells. Usually fibroblast growth factor

Extramedullary haematopoiesis occurs in other areas such as the liver and spleen leading to hepatomegaly and splenomegaly. This can lead to portal hypertension. If it occurs around the spine it can lead to spinal cord compression.

61
Q

How may myeloproliferative disorders present?

A

Myelofibrosis leads to low RBC, WBC and platelets

  • Firstly asymptomatic
  • Systemic symptoms: fatigue, weight loss, night sweats, fever
  • Anaemia (except in polycythaemia)
  • Splenomegaly (abdominal pain)
  • Portal hypertension (ascites, varices and abdominal pain)
  • Low platelets (bleeding and petechiae)
  • Thrombosis is common in polycythaemia and thrombocythaemia
  • Raised red blood cells (thrombosis and red face)
  • Low white blood cells (infections)
62
Q

What are the three main symptoms of polycythaemia vera?

A
63
Q

What are the FBC findings in myeloproliferative disorders?

A
64
Q

If you suspect myelofibrosis what investigations should you order and what will these investigations show?

A

Blood film

  • Teardrop shaped RBCs
  • Varying sizes of RBCs
  • Immature red and white cells (blasts)

Diagnosis

Bone marrow biopsy as bone marrow aspiration is usually dry as scar tissue

Testing for the JAK2, MPL and CALR genes can help guide management

65
Q

How is primary myelofibrosis managed?

A
  • Patients with mild disease with minimal symptoms might be monitored and not actively treated
  • Allogeneic stem cell transplantation is potentially curative but carries risks
  • Chemotherapy can help control the disease, improve symptoms and slow progression but is not curative on its own
  • Supportive management of anaemia, splenomegaly and portal hypertension
  • JAK2 inhibitors and hydroxycarbamide
66
Q

How is polycythaemia vera managed?

A
  • Venesection is first line, Hct<0.45
  • Aspirin 75mg daily to reduce risk of VTE
  • Cytoreductive therapy/Hydroxycarbamide to control the disease
67
Q

How is essential thrombocythaemia managed?

A
  • Aspirin
  • Chemotherapy/Cytoreductive therapy if high risk of transformation
68
Q

What are some causes of polycythaemia?

A

Raised haemtocrit

Primary: Polycythaemia Vera

Secondary: see image

Relative: Decrease in plasma volume e.g dehydration, diuretics

69
Q

What is the main mutation in polycythaemia vera?

A

JAK2 - Tyrosine Kinase

70
Q

How is polycythaemia vera usually detected?

(image important)

A
  • Incidental finding on FBC and asymptomatic

OR

  • Symptoms of raised haematocrit with gradual onset e.g hypertension
71
Q

What is erythromelalgia?

A
72
Q

What investigations are done to find out the underlying cause of polycythaemia?

A

Iron deficiency can mask polycythaemia vera

73
Q

What is the diagnostic criteria for polycythaemia vera?

A
  • High haematocrit (> 0.52 in men, > 0.48 in women) OR raised red cell mass (>25% above predicted)
  • AND*
  • Mutation in JAK2
74
Q

What is the prognosis with polycythaemia vera?

A
  • If untreated survival is 18 months
  • If treated can live several decades
  • 5% transform for AML
  • 5-15% progress to myelofibrosis by 15 years
75
Q

What are some causes of thrombocythemia apart from essential thrombocythaemia?

A
  • Do bone marrow biopsy
  • Do iron studies
  • Blood film
76
Q

How does essential thrombocythemia present and what investigations would you do and what would they show?

A
  • Burning sensation in hands
  • Thrombosis
  • Haemorrhage – more common if plt count >1500
  • Splenomegaly
  • Platelet count > 600 * 109/l
  • JAK2 mutation in 50% of patients
77
Q

What is myelodysplasia?

A

Pre-Leukaemia - may progress to AML

Myeloid bone marrow cells not maturing properly. Bone marrow hyper cellular but peripherally pancytopenic

Cause anaemia, neutropenia, thrombocytopenia

78
Q

What types of patients is myelodysplasia more common in?

A
  • Above 60
  • Previous radio/chemotherapy

There is an increased risk of transforming into acute myeloid leukaemia

79
Q

How may myelodysplasia present and how is it diagnosed?

A

Presentation

  • Asymptomatic and found incidentally on FBC
  • Symptoms of anaemia (fatigue, pallor or shortness of breath), neutropenia (frequent or severe infections) or thrombocytopenia (purpura or bleeding)

Diagnosis

  • FBC abnormal
  • Blasts on blood film
  • Confirmed by bone marrow aspiration and biopsy
80
Q

How is myelodysplasia managed?

A
  • Watchful waiting
  • Supportive treatment with blood transfusions if severely anaemic
  • Chemotherapy
  • Stem cell transplantation
81
Q

What is the logic behind watch and wait in early CLL and CML?

A
  • The use of alkylating agents or aggressive chemotherapy in patients with early-stage disease does not prolong survival
  • There are risks of early treatment, including potential side effects and treatment complications.
  • Patients may build up a resistance to the drugs used and would not be able to use them again when treatment for progressive disease is necessary.
82
Q

What is the most common leukaemia in children?

A

ALL

(AML if Downs)

Y4 Cancer Care (19 decks)

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