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7. Haematology > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

What is leukaemia?

A

A malignant proliferation of haemopoietic stem cells.

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2
Q

Name 4 sub-types of leukaemia.

A
  1. AML - acute myeloid leukaemia.
  2. CML - chronic myeloid leukaemia.
  3. ALL - acute lymphoblastic leukaemia.
  4. CLL - chronic lymphoblastic leukaemia.
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3
Q

Give 3 environmental causes of leukaemia.

A
  1. Radiation exposure.
  2. Chemicals e.g. benzene compounds.
  3. Drugs.
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4
Q

Give 5 symptoms of leukaemia.

A
  1. Anaemia.
  2. Infection and neutropenia
  3. Bleeding.
  4. Hepatomegaly.
  5. Splenomegaly.
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5
Q

Give 5 signs of leukaemia.

A
  1. Pallor, fatigue
  2. SOB
  3. Angina
  4. Claudication
  5. Infections and Fever
  6. Mouth ulcers
  7. Bleeding under the skin
  8. Bruising and Petechiae
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6
Q

Why are hepatomegaly and splenomoegaly symptoms of leukaemia?

A

Because of tissue infiltration.

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7
Q

Why are anaemia, infection and bleeding symptoms of leukaemia?

A

Because of bone marrow failure.

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8
Q

What investigations might you do on someone who you suspect has leukaemia?

A
  1. Blood film.
  2. Bone marrow biopsy.
  3. Lymph node biopsy.
  4. Immunophenotyping.
  5. Cytogenetics.
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9
Q

What is acute myeloid leukaemia (AML)?

A

Neoplastic proliferation of blast cells derived from marrow myeloid – Myeloblasts (gives rise to basophils, neutrophils and eosinophils) elements

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10
Q

What can increase the risk of developing AML?
Give 3 risk factors.

A
  1. Preceding haematological disorders - can be a transformation from a myeloproliferative disorder.
  2. Prior chemotherapy.
  3. Exposure to ionising radiation.
  4. Age.
  5. Down Syndrome.
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11
Q

What is the typical age of onset of AML?

A

Around 65

Most common adult leukaemia.

5yr survival 25%

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12
Q

What cell lines are affected in acute myeloid leukaemia (AML)?

A

Blast cells.

Clonal expansion of myeloid blasts in the bone marrow, peripheral blood or extramedullary tissue.
Unable to differentiate into neutrophils.

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13
Q

List some conditions/RFs associated with AML

A

Myelodysplastic syndrome (MDS).
Down Syndrome.
Bone marrow failure syndromes (e.g. Fanconi, Diamon-Blackfan, aplastic anaemia)
Smoking.

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14
Q

What is the state of RBC, WBC and platelets in leukaemia?

A
  1. Anaemia – low Hb
  2. Neutropenia – low WCC
  3. Thrombocytopenia – low platelets
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15
Q

How would you diagnose AML?

A
  1. Full blood count – initial 1st line investigation
    - WCC usually high
    - Neutropenia, Thrombocytopenia, Anaemia
  2. Blood film
    - Blast cells, Auer rods
  3. Blood coagulation tests
    - Elevated PT time (prothrombin time)
    - Normal fibrinogen and D-dimer
  4. Bone marrow biopsy – definitive investigation for diagnosis!!
    - Auer rods, hypercellularity
    - Aspirate biopsy (>20% myeloblasts = diagnostic)
  5. Imaging – CXR, CT, MRI, PET scanning
    - CXR pulmonary infiltrates
  6. Immunophenotyping – cell markers – myeloid? lymphoid? B-cell? T-cell?
  7. Molecular methods
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16
Q

Which investigation is the definitive test for AML? And what does it find for positive AML?

A

Bone marrow biopsy – definitive investigation for diagnosis
- Auer rods, hypercellularity
- Aspirate biopsy (>20% myeloblasts = diagnostic)

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17
Q

Treatment for AML: briefly list the 3 methods of AML management.

A
  1. Supportive care.
  2. Chemotherapy: curative v palliative.
  3. Bone marrow transplant.
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18
Q

How would you manage/treat AML?

A

Supportive care:
1. IV fluids for hydration
- Hickman line -> easily take bloods for testing, administer
drugs + fluids

  1. Prophylactic antivirals, antibacterials and antifungals
    - Deadly infections caused by neutropenia
    - E.G. acyclovir, fluconazole, ciprofloxacin, co-trimoxazole
  2. Blood + platelet transfusions, as needed
  3. Allopurinol
    - Prevent tumour lysis syndrome
  4. Leukoreduction
    - Hydroxycarbamide/leukapheresis

Chemotherapy – Induction:
1. Cytarabine + an anthracycline (daunorubicin)

  1. All-trans retinoic acid added in APML

Stem cell bone marrow transplant.

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19
Q

What drugs can be used in chemotherapy for AML?

A
  1. Cytarabine + an anthracycline (daunorubicin)
  2. All-trans retinoic acid added in APML cancer
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20
Q

Give the main complication of AML.

A
  1. Infection is a major issue - be alert to septicaemia.
    Causes common organisms to present oddly, with few antibodies being made.
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21
Q

What is CML?

A

Chronic myeloid leukaemia.

Uncontrolled clonal proliferation of myeloid cells (basophils, eosinophils and neutrophils) in the BM.

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22
Q

What cell lines are affected in CML?

A

Myeloid - uncontrolled proliferation of myeloid cells in BM.

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23
Q

What would the FBC from someone with CML look like?

A

High WBC’s.

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24
Q

What chromosome is present in >80% of people with CML?

A

Philadelphia chromosome.

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25
Q

Explain why the Philadelphia chromosome causes CML.

A

Philadelphia chromosome leads to a fusion gene that has tyrosine kinase activity and enhanced phosphorylating activity -> altered cell growth.

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26
Q

What are the genetics/pathophysiology behind CML?

A

Philadelphia chromosome - translocation between chromosomes 9 and 22 - t(9;22).

1) Ph chromosome produced BCR-ABLE fusion oncogene
2) Produces p210 BCR-ABL protein
3) Expressive active tyrosine kinase on surface of myeloid cells
4) Unregulated cell division

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27
Q

Pathophysiology of CML: how many phases of CML are there?

A

3 typical phases: the chronic phase, the accelerated phase and the blast phase.

28
Q

Pathophysiology of CML: describe the chronic phase of CML.

A

The chronic phase can last around 5 years, is often asymptomatic and patients are diagnosed incidentally with a raised WCC.

29
Q

Pathophysiology of CML: describe the accelerated phase of CML.

A

The accelerated phase occurs where the abnormal blast cells take up a high proportion of the cells in the BM and blood (10-20%). In the accelerated phase, patients become more symptomatic, develop anaemia + thrombocytopenia and become immunocompromised.

30
Q

Pathophysiology of CML: describe the blast phase of CML.

A

The blast phase follows the accelerated phase and involves an even high proportion of blast cells and blood (>30%). This phase has severe symptoms and pancytopenia. It is often fatal.

31
Q

Describe the clinical features of CML

A

1/3 asymptomatic at presentation.

early symps - weight loss, malaise, fever, night sweats, abdo discomfort (due to splenomegaly), arthralgia (increased uric acid from cell turnover)

in 10% the chronic phase will turn into a symptomatic accelerated phase, or blast phase (AML).

32
Q

What investigations would you do in CML?
What results would you expect to see?

A
  1. Full blood count – initial 1st line investigation
    - Very high WCC - with whole spectrum of myeloid cells i.e. increased; neutrophils, myelocytes, basophils and eosinophils
    - Anaemia - Low Hb (normochromic and normocytic)
    - Platelets are low, normal or raised
  2. BM aspiration biopsy
    - Granulocytic hyperplasia – hypercellular
  3. Cytogenetic analysis – FISH
    - Presence of Philadelphia chromosome
33
Q

How would you treat CML?

A
  • Chronic/accelerated phase:
    o Tyrosine kinase inhibitors (imatinib)
  • SEs = muscle cramps/HF.
    o May be combined with IFN-α, if required
    o High-dose induction chemo and allogenic stem cell transplant, if above fails
  • Blast phase:
    o Tyrosine kinase inhibitor + high dose chemo followed by stem cell transplantation
    o May have pancytopenia, requiring blood and platelet transfusion
    o Death imminent if this does not work
34
Q

What is the main medication for CML treatment?

A

Tyrasine kinase inhibitors.

35
Q

What is ALL?

A

Acute lymphoid leukaemia.
Malignancy of immature lymphoid precursor cells (gives rise to T cells and B cells).

36
Q

What cell lines are affected in ALL?

A

Lymphoblasts - B/T cell precursors. lymphoid cells replace haematopoietic cells.

37
Q

Name a trigger of ALL.

A

Ionising radiation during pregnancy.

38
Q

Is ALL more common in adults or children?

A

ALL is mainly a childhood disease.

39
Q

Describe the pathophysiology of ALL.

A
  • Malignant change in lymphoblast (lymphoid precursor cell – I.E. precursor for B or T cells)
  • Promotes uncontrolled, rapid proliferation of immature lymphoblasts in the BM
  • Affects a single type of lymphocyte (either T or B lymphocyte cell lines)
  • Causes acute proliferation of a single type of lymphocyte
  • Excessive proliferation of these cells causes them to replace the other cell types being created in the BM, leading to a pancytopenia.
  • Majority of cases derive from B-cell precursors
  • If all B cells = CHILDREN
  • If all T cells = Adults
40
Q

Give 4 symptoms of ALL.

A
  1. Bone pain.
  2. Recurrent infections (neutropenia).
  3. Pale and tired (anaemia).
  4. Bruising and bleeding (low platelets).
  5. Swollen testicles.
  6. Cranial nerve palsies and neck stiffness.
41
Q

What CNS involvement can you get in ALL?

A

CNS infiltration by leukaemoid cells presents as papilloedema, nuchal rigidity and meningism.

Also might get focal neurology CN 3, 4, 6, 7

42
Q

Outline 3 classification systems used in ALL.

A

FAB (french/american/british):

  • L1 - small homogenous blasts (children)
  • L2 - large heterogenous blasts (adults)
  • L3 - Burkitt large basophilic B cells with vacuoles

Immunological - uses surface markers
Cytogenetic - chromosomal analysis, Ph chromosome is a poor prognosis.

43
Q

What infections are commonly seen in ALL patients?

A

CMV, measles, candidiasis, Pneumocystis pneumonia (PCP)

44
Q

What investigations would you carry out on an ALL patient?
What would the results show?

A
  1. History
  2. Examination
  3. Full blood count – initial 1st line investigation
    - WCC usually high
  4. Blood film
    - Blast cells on film + in BM
  5. Bone marrow biopsy – definitive investigation for diagnosis!!
    - Aspirate and trephine
  6. Imaging – CXR, CT, MRI, PET scanning
    - CXR and CT scan to look for mediastinal and abdominal lymphadenopathy
  7. Lumbar puncture
    - To look for CNS involvement
  8. Immunophenotyping – cell markers – myeloid? lymphoid? B-cell? T-cell?
  9. Cytogenetics/FISH
  10. Molecular studies
45
Q

List the 2 treatment options for ALL.

A

CNS directed therapy and stem cell transplant.

46
Q

How would you treat ALL?

A

Supportive care:
1. Prophylactic antivirals, antibacterials and antifungals
- Deadly infections caused by neutropenia
- E.G. acyclovir, fluconazole, ciprofloxacin, co-trimoxazole
2. IV fluids for hydration
- Hickman line -> easily take bloods for testing, administer drugs + fluids
3. Blood + platelet transfusions
4. Allopurinol
- Prevent tumour lysis syndrome

Chemotherapy – CNS directed therapy:
1. Prednisolone, vincristine, daunorubicin + tyrosine kinase inhibitor (imatinib)
2. Intrathecal methotrexate (for CNS disease)

Stem cell bone marrow transplant

Consolidate remission (weeks).
Maintain remission (years).
- Mercaptopurine daily, MTX weekly, vincristine + pred monthly.

47
Q

List some potential complications of ALL.

A
  1. Tumour lysis syndrome
  2. Neutropenic sepsis
  3. Pancytopenia
  4. Chemotherapy SEs
48
Q

What is CLL?

A

Chronic lymphoid leukaemia.

Chronic proliferation of a single-type of well-differentiated lymphocyte, usually B lymphocytes, which leads to the accumulation of mature B-cells that have escaped apoptosis.

49
Q

Who does CLL affect?

What is the prognosis like?

A

An incurable disease of older people - but some show no/slow progression - have a near normal life expectancy.
(others show active progression so have a worse prognosis).

Most common leukaemia.

50
Q

What cell lines are affected in CLL?

A

Mature B cells - they have escaped apoptosis.

51
Q

What can trigger CLL?

A

Pneumonia

52
Q

Name 3 risk factors for CLL.

A
  1. Male sex
  2. Genetics – Mutations, trisomies and deletions influence risk
  3. Pneumonia may be a triggering event
53
Q

Give some clinical features of CLL.

A
  • Often asymptomatic (can present as a surprise on routine FBC)
  • May be anaemic (due to haemolysis or marrow infiltration)
  • Infection prone
  • Bleeding
  • If severe, then weight loss, sweats and anorexia
  • Hepatosplenomegaly
  • Enlarged, rubbery, non-tender nodes
  • Painless, rubbery lymphadenopathy
54
Q

How would you investigate CLL?

A
  1. Full blood count – initial 1st line investigation
    - Normal or low Hb + platelets
    - Raised WCC with very high lymphocytes (lymphocytosis)
  2. Blood film
    - Smudge cells / Smear cells may be seen in vitro
    - These occur during the process of preparing the blood film where aged or fragile WBCs rupture and leave a smudge on the film.
  3. Flow cytometry
    - CD5, CD19, CD23 positive
  4. CT scan
    - Hepatosplenomegaly, retroperitoneal/mediastinal lymph nodes
55
Q

Outline staging of CLL and how it influences treatment plans.

A

Binet:

  • A: <3 nodes + normal Hb and Pt
  • B: >=3 nodes + normal Hb and Pt
  • C: anaemia/thrombocytopenia + any nodes.

Rx:
A+B+asymptomatic = watch and wait, monitor FBC, flow cytometry every 3/12
C = chemo - rtirxuimab + cyclophosphamide + fludarabide +/- stem cell transplant

56
Q

What is the treatment for CLL?

A
  1. Do nothing.
  2. Blood transfusions.
  3. Human IV immunoglobulins
  4. Chemotherapy or Radiotherapy
  5. mAb.
  6. Bone marrow / stem cell transplant.
57
Q

What are 2 main complications to worry about in CLL?

A

1) Hypogammaglobulinaemia.
= Lymphocytes don’t work = no antibodies - so patient is deficient in IgG/A/M = increased infection risk.

  • May need monthly IVIG

2) Autoimmune haemolytic anaemia.
= Dysfunctional antibodies directed towards RBCs.

  • Give prednisolone.
58
Q

For CLL, what is the prognosis rule?

A

Rule of 3’s:
* 1/3 will never progress
* 1/3 progress slowly
* 1/3 progress actively

59
Q

Give some clinical features of acute leukaemias.

A

Marrow failure - anaemia symptoms, infections e.g. candida (neutropaenia), bleeding/petechial rash (thrombocytopaenia).

Circulating cell symptoms - headache, CNS involvement (cranial nerves). Infiltration: skin/gums (some AMLs), hepatosplenomegaly, lymphadenopathy, testicular enlargement.

Tumour related symptoms - bone pain, fever, lethargy and fatigue, night sweats, weight loss.

60
Q

Which leukaemia most commonly affects children?

A

ALL - acute lymphoblastic leukaemia

Rare in adults (75% is under <6yrs old). two spikes again in mid 30s and mid 80s

90% will have complete remission (if <30yo)

61
Q

Which of the leukaemias doesn’t cause recurrent infections?

A

CML - chronic myeloid leukaemia

62
Q

Which leukaemia commonly affects the elderly?

A

CML

63
Q

Which of the leukaemias is most associated with Down’s syndrome?

A

ALL - acute lymphoblastic leukaemia

64
Q

If you see blast cells on a blood film, what does this suggest?

A

An acute leukaemia

65
Q

If Auer rods are seen on a blood film, which leukaemia is this?

A

AML

66
Q

If smudge cells are seen on a blood film, which leukaemia is this?

A

CLL

7. Haematology (15 decks)

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