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Yr 5 - Haematology > Revision - Leukaemia > Flashcards

Revision - Leukaemia Flashcards

1
Q

What cells are involved in chronic vs acute leukaemias?

A

Acute - uncontrolled proliferation of myeloid/lymphoid progenitor cells

Chronic - uncontrolled proliferation at a later stage of differentiation

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2
Q

What type of leukaemia is most commonly seen in paeds?

A

ALL

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3
Q

What genetic abnormality is seen in 90% of CML cases?

A

Philadelphia chromosome

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4
Q

What is the Philadelphia chromosome?

A

This results from a translocation between chromosomes 9 and 22, t(9;22).

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5
Q

Most common type of ALL?

A

B cell ALL

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6
Q

What is the most common childhood malignancy?

A

ALL

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7
Q

What age does ALL peak?

A

2-3 y/o

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8
Q

How much more likely are patients with Down’s syndrome likely to develop ALL & AML?

A

ALL - 30x more likely

AML - 150x more likely

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9
Q

What type of leukaemia is most associated with Down’s syndrome?

A

AML

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10
Q

What 2 viruses can predispose to leukaemia?

A

EBV & HIV

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11
Q

Clinical features of ALL?

A

1) Organomegaly:
- hepatomegaly
- splenomegaly

2) Fever, night sweats & weight loss

3) Lymphadenopathy

4) Thrombocytopenia:
- unusual bleeding/bruising
- petechial rash

5) Anaemia:
- pallor
- persistent fatigue
- syncope

6) Bone pain

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12
Q

Cause of organomegaly in ALL?

A

Lymphoblast infiltration of other organs leads to clinical features of organomegaly.

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13
Q

1st line investigation in suspected ALL?

A

FBC with a differential

This will highlight haematological derangements due to increased circulating lymphoblasts and bone marrow suppression

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14
Q

Cause of pancytopenia in ALL?

A

Due to bone marrow suppression (due to overproduction of one cell type)

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15
Q

FBC in ALL?

A

1) Thrombocytopenia (75%)

2) Anaemia (50%)

3) WBC can either be low (50%), high (20%), or normal if bone marrow is not yet suppressed
- differential count usually reveals neutropaenia

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16
Q

What does a low WBC vs high WBC count in ALL indicate?

A

Low WBC –> indicates that although there are lymphoblasts present they have not achieved sufficient differentiation to be recognised as WBC

High WBC –> indicates they have properties similar enough to a mature WBC to be counted.

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17
Q

What further investigations are required in any case presenting with suspected ALL to screen for complications?

A

Identifying complications:

1) Infection screen

2) Coagulation profile

3) U&Es, LDH & uric acid–> identify any metabolic abnormalities or tumour lysis syndrome.

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18
Q

Next investigation to diagnose ALL that is required in the presence of an abnormal FBC result?

A

Peripheral blood smear –> to examine circulating lymphoblasts

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19
Q

On a bone marrow biopsy, what is the most commonly accepted threshold for diagnosis ?

A

When lymphoblasts occupy >20% of bone marrow.

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20
Q

Give 2 red flags that would warrant an urgent specialist assessment for suspected haematological malignancy in children

A

1) unexplained petechiae

2) unexplained hepatosplenomegaly

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21
Q

Give some red flags that would warrant an urgent FBC for suspected haematological malignancy in children

A

1) Pallor
2) Persistent fatigue
3) Unexplained fever
4) Unexplained persistent infection
5) Generalised lymphadenopathy
6) Unexplained bruising or bleeding
7) Persistent/unexplained bone pain

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22
Q

What is highly suspicious for leukaemia if seen on microscopy?

A

Blast cells (immature cells)

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23
Q

What may a cogulation profile show in leukaemia?

A

May be deranged or show disseminated intravascular coagulation (DIC).

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24
Q

Why is a baseline kidney & liver function important in leukaemia?

A

These are needed prior to starting chemotherapy.

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25
Q

What may LDH & uric acid levels show in leukaemia?

A

Raised lactate dehydrogenase and uric acid occur with increased cell turnover.

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26
Q

Why is G6PD level important in leukaemia?

A

Treatment with rasburicase in G6PD deficiency can result in haemolytic crisis.

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27
Q

What is rasburicase?

A

Drug given before and during chemo that can help prevent tumour lysis syndrome.

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28
Q

What drug can help prevent tumour lysis syndrome?

A

Rasburicase

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29
Q

At the end of induction chemotherapy in leukaemia, what should the blast cell count be for patients to be classed as being in remission?

A

≤5%

Presence of residual disease (i.e. persistent leukaemic cells) indicates the need for more intensive chemotherapy

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30
Q

What are the 4 stages of chemo for ALL?

A

1) Induction

2) Consolidation and CNS treatment

3) Delayed intensification

4) Maintenance

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31
Q

What is the induction phase of chemo?

A

What - An intensive phase lasting 4-6 weeks.

Purpose - Aims to destroy all leukaemic blast cells.

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32
Q

To reduce the risk of tumour lysis syndrome in chemo for leukaemia, what can be given prior to induction?

A

Pre-treatment with hydration & allopurinol/rasburicase

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33
Q

What is the aim of the consolidation and CNS treatment stage of chemo for ALL?

A

Maintain remission

LP with intrathecal methotrexate aims to prevent spread to CNS

34
Q

What mx is used in leukaemia to prevent CNS spread?

A

Intrathecal methotrexate

35
Q

What is the aim of the ‘delayed intensification’ stage of chemo for ALL?

A

To remove as many remaining blasts as possible prior to the maintenance phase.

36
Q

How long does treatment for ALL continue for in boys vs girls (i.e. the maintenance phase)?

A

Girls - 2y

Boys - 3y

37
Q

What is tumour lysis syndrome?

A

As lymphoblasts lyse and release their contents, this leads to deranged metabolic abnormalities.

  • hyperkalaemia
  • hypocalcaemia
  • hyperuricaemia
  • hyperphosphataemia
38
Q

Mx of tumour lysis syndrome?

A

Rapid rehydration with IV fluids, allopurinol and close monitoring.

39
Q

Which chemo agent used in leukaemia can cause cardiotoxicity?

A

Anthracyclines e.g. doxorubicin

40
Q

What are the clinical manifestations of tumour lysis syndrome?

A

1) AKI

2) Cardiac arrhythmias

3) N&V

4) Seizures

41
Q

When can rasburicase be used in prophylactic management of tumour lysis syndrome?

A

If WCC >50

42
Q

Mechanism of rasburicase vs allopurinol in tumour lysis syndrome?

A

Allopurinol - prevents uric acid production

Rasburicase - actively breaks down uric acid

43
Q

What should always be EXCLUDED before giving rasburicase?

A

G6PD deficiency - as it increases the risk of haemolytic crisis.

44
Q

ALL can cause organomegaly (hepatomegaly (64%) or splenomegaly (61%)).

How may this present?

A
  • anorexia
  • weight loss
  • abdo pain
  • abdo distension
45
Q

How does lymphadenopathy typically present in ALL?

A

A persistent or progressive, painless, firm, rubbery lymph node.

46
Q

What 2 types of leukaemias are most common in children?

A

ALL & AML

47
Q

Peak incidence age of AML?

A

70+ y/o

48
Q

Pathophysiology of AML?

A

clonal expansion of myeloid progenitor cells in the bone marrow

49
Q

Clincial features of AML?

A

1) Fever

2) Anaemia symptoms

3) Thrombocytopenia
- Ecchymoses or petechiae.
- Gingival bleeding, epistaxis, or menorrhagia.

4) Coagulopathy
- Bleeding secondary to DIC

5) Bone pain

6) Gingival hypertrophy:

7) CNS involvement:
- Headache, visual changes, and nerve palsies.

8) Organomegaly

50
Q

Onset of symptoms in AML?

A

There is sudden onset of symptoms and it progresses rapidly

51
Q

Cuase of bone pain in leukaemia?

A

Due to expansion of the medullary cavity by the leukemic process.

52
Q

1st & 2nd line investigations in AML?

A

1) FBC with differential

2) Peripheral blood smear

53
Q

What will be seen on FBC with differential in AML?

A
  • Normocytic, normochromic anaemia
  • Thrombocytopenia
  • Leucocyte count: maybe low, normal, or raised.
54
Q

What may be seen on a peripheral blood smear in AML?

A

1) Raised myeloblasts

2) Auer rods

55
Q

What are myeloblasts?

A

immature cells with large nuclei

56
Q

What are auer rods?

A

Pink/red, rod-shaped cytoplasmic granular inclusions.

These are pathognomonic of myeloblasts.

57
Q

What do auer rods indicate?

A

AML

58
Q

What % of myeloblasts in the bone marrow confirms the diagnosis of AML?

A

≥20%

59
Q

What is acute promyelocytic leukaemia (APL)?

A

a distinct subtype of AML that represents a medical emergency.

60
Q

Give some complications of leukaemia

A

1) Tumour lysis syndrome

2) Leukostasis

3) DIC

4) Severe neutropenia

5) Severe thrombocytopenia

6) Severe anaemia

7) VTE

61
Q

What is leukostasis?

A

Excessive number of leukaemic cells causes increased blood viscosity.

It typically presents with respiratory or neurological distress.

The clinical features are:
- Chest pain
- Headache
- Altered mental status
- Priapism

62
Q

What age is associated with favourable prognosis in AML?

A

<50

63
Q

What occurs in CLL?

A

due to monoclonal proliferation of B-lymphocytes.

64
Q

What is the most common form of leukemia found in adults in Western countries?

A

CLL

65
Q

Peak age of CLL?

A

60-70 y/o

66
Q

Onset of symptoms in CLL?

A

Slow onset

More than 50% cases are often diagnosed coincidentally following routine blood tests.

67
Q

Clinical features of CLL?

A

1) Symmetrical lymphadenopathy in the neck, armpits or groin

2) Hepatomegaly and/or splenomeglay
- abdo discomfort

3) Anaemia

4) Thrombocytopenia

5) Infections

68
Q

What are ‘B symptoms’?

A

A sign that CLL may be active:

1) Frequent, severe night sweats

2) Unexplained weight loss >10% of body weight in the previous 6 months

3) High fever in the absence of any infections (>38°C)

69
Q

Investigations in CLL?

A

1) FBC –> absolute lymphocytosis

2) Peripheral blood smear –> confirm lymphocytosis

70
Q

What staging system is commonly used in the UK for CLL staging?

A

Binet staging system

71
Q

When is chemo indicated in CLL?

A

should only be given to patients with active, symptomatic disease

72
Q

For a small number of people, CLL can sometimes transform into a different type of cancer.

What is this referred to as?

A

Richter transformation

73
Q

What is Richter transformation?

A

A serious complication of CLL and if often fatal.

It is characterised by the sudden transformation of the CLL into a significantly more aggressive form of large cell lymphoma.

74
Q

Symptoms of Richter transformation?

A

1) a sudden and dramatic increase in the size of lymph nodes characterised by usually painless areas of swelling in the neck, axilla, abdomen (spleen) or groin.

2) a dramatic unexplained weight loss, fevers and night sweats (B-symptoms).

75
Q

Patients with CLL have a higher risk of developing a secondary malignancies than the general population.

What malignancies are seen most frequently?

A
  • melanoma
  • soft tissue sarcoma
  • colorectal cancer
  • lung cancer
  • squamous cell skin cancer
  • basal cell carcinoma
76
Q

Peak incidence age of CML?

A

60-70 y/o

77
Q

What is the hallmark genetic abnormality in CML?

A

The presence of the BCR-ABL fusion gene.

This results from a reciprocal translocation between chromosomes 9 and 22, known as the Philadelphia chromosome.

78
Q

FBC results in CML?

A

1) Leucocytosis

2) The differential may demonstrate increased cell numbers from the myeloid lineage of leucocytes.

3) Thrombocytosis or thrombocytopenia may occur

4) Anaemia is a common finding, often normochromic and normocytic

79
Q

What is the most common treatment for CML?

A

Tyrosine kinase inhibitors e.g. imatinib

80
Q

1st line tyrosine kinase inhibitor in CML?

A

imatinib

81
Q
A

Yr 5 - Haematology (9 decks)

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