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Gwen - Haematology > Acute Lymphoblastic Leukaemia > Flashcards

Acute Lymphoblastic Leukaemia Flashcards

1
Q

What is acute lymphoblastic leukaemia?

A

https://www.youtube.com/watch?v=itkRVTqfPsE

Malignancy of lymphoid cells, affecting T or B cell lines, arresting maturation and promoting uncontrolled proliferation of immature blast cells, with marrow failure and tissue infiltration. Affects the progenitor cells.

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2
Q

What are known causes of ALL?

A

Precise cause unknown

  • Prenatal Ionizing radiation
  • In utero exposure to infection
  • Environmental radiation
  • Down’s Syndrome
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3
Q

Who does ALL most commonly affect?

A

Children - rare in adults

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4
Q

What proportion of ALL are of B-cell lineage?

A

75-90%

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5
Q

How does ALL present?

A

Marrow failure

  • Anaemia (fatigue)
  • Thrombocytopenoa
    • Purpura and mucosal bleeding
    • Bruises and petichae
    • Subconjunctival haemorrhage
  • Neutropenia - fever + infection

Infiltration

  • Anorexia
  • Bone pain (due to amrrow expansion)
  • Painless lumps - Neck, axilla, groin
  • Infiltration - Hepatosplenomegaly, lymphadenopathy, orchidomegaly, CNS involvement IS COMMON eg cranila nerve palsies, meningism
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6
Q

What are signs of thrombocytopenic bleeding?

A
  • Petechiae/Purpura
  • Mucosal bleeding - gums
  • Fundal haemorrhage
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7
Q

What are the commonest infections that occur in ALL?

A

Chest, mouth, perianal, skin

  • Bacterial septicaemia
  • Herpes Zoster
  • CMV
  • Measles
  • Candidiasis
  • Pneumocystis Pneumonia
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8
Q

What are the following?

A

Petechiae - Small (1–2 mm) haemorrhages into mucosal or serosal surfaces

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9
Q

What are causes of the following?

A
  • Thrombocytopenia of any cause - autoimmune, heparin-induced, hypersplenism
  • Bone marrow failure - malignancy
  • Defective platelet function
  • DIC
  • Infection
  • Bone marrow defects
  • Factor deficiencies
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10
Q

What is the following?

A

Purpura - >3 mm haemorrhages, or when ecchymoses and petechiae form in groups

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11
Q

What are causes of the following?

A

Diseases associated with:

  • Trauma
  • Vasculitis – particularly palpable purpura
  • Amyloidosis
  • Over-anticoagulation
  • Factor deficiencies
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12
Q

What is the mechanism of colour change in bruising?

A

Erythrocyte -> Bilirubin (blue/green) -> Haemosiderin (yellow)

Once under the skin, erythrocytes are phagocytosed and degraded by macrophages, with haemoglobin converted to bilirubin (blue–green discolouration).

Bilirubin is eventually broken down into haemosiderin (which is golden brown) at the end of the process before skin returns to its normal hue.

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13
Q

What CNS involvement can occur in ALL?

A
  • Cranial nerve palsies
  • Meningism
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14
Q

What are poor prognostic factors for ALL?

A
  • Age > 60yrs - “dreadful”
  • White cell count > 300 x 109/L
  • Immunophenotype (more primitive forms)
  • Cytogenetics/molecular genetics - Philedelphia chromosome t(9;22); t(4;11)
  • Slow/poor response to treatment
  • Presentation with CNS signs
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15
Q

How would you investigate suspected ALL?

A
  • Bloods - FBC, U+E’s, LFTS, LDH, Urate, Coagulation screen, Blood film
  • Bone marrow
  • CXR
  • CT Scan
  • Consider LP?
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16
Q

What might you see on FBC in someone with ALL?

A
  • Normochromic, normocytic anaemia
  • WBC raised usually (sometimes normal or low)
  • Platelets low
17
Q

What might you see on Blood film in someone with ALL?

A

Blast cells almost invariably seen

18
Q

What proportion of bone marrow needs to be blast cells for the diagnosis of ALL to be made?

A

>20%

Note tha biopsy defines this condition.

19
Q

How quickly does ALL present?

A

2-3 weeks of bone marrow failure plus bone/joint pain

20
Q

Why does someone with ALL get bone pain?

A

Bone fills up with blast cells

21
Q

What is the prognosis for ALL?

A
  • Cure rate children - 70-90%
  • Cure rate adults - 40%
22
Q

Why would you do a CXR in ALL?

A

Look for mediastinal widening which is characteristic of T-cell lymphoblastic leukaemia

23
Q

Why would you consider doing an LP in someone with ALL?

A

Look for signs of CNS involvement

24
Q

Why would you do a bone marrow biopsy in suspected ALL?

A

Look for:

  • Increased cellularity, reduced erythropoiesis, reduced megakaryocytes.
  • Replacement by blast cells >20%
  • Lineage confirmation by immunophenotyping
    • B lineage ALL – CD10 and CD19
    • T lineage ALL– CD3
  • Cytogenetic FISH analysis in real-time PCR
25
Q

How would you manage someone with ALL?

A
  • Supportive Therapy
    • ​Blood/platelet transfusion
    • IV fluids
    • Allpurinol (prevents tumour lysis syndrome)
  • Infections
    • ​Immediate IV abx when infection, prohylacctic antivirals/antifungals.
  • Induction chemotherapy + CNS directed treatment
  • Steroids in emergency
  • Consolidation therapy
  • Maintenance treatment for 18 months
  • Stem cell transplantation (if high risk)
26
Q

What chemotherapeutic medications are used for induction chemotherapy?

A

Over 4 weeks:

  • Vincristine
  • Dexamethasone
  • L-asparaginase
  • Daunorrubicin - high risk patients
27
Q

What CNS prophylaxis would you use?

A

Intrathecal methotrexate +/- CNS irradiation (if known CNS involvement)

28
Q

What is involved in consolidation therapy?

A

High-medium dose therapy in blocks over several weeks

29
Q

Where is relapse of ALL most commonly found?

A
  • Blood
  • CNS
  • Testis
30
Q

What complications can arise from ALL?

A
  • Neutropenic sepsis
  • Hyperuricaemia - from massive cell death
  • Poor growth
  • CNS tumour
31
Q

What might you find on investigation of serum urate and LDH in ALL?

A

Both increased

32
Q

What might you find on CSF in someone with ALL?

A
  • Pleocytosis (with blast cells)
  • Increased protein
  • Decreased glucose
33
Q

What genetic disorder is associated with development of ALL, and how much does this disorder increase the risk of developing ALL?

A

Down’s syndrome - 4-fold increase

34
Q

What age range is the peak incidence of ALL?

A

2-6 years. Second peak after 50 years

35
Q

What supportive therapy would you use in ALL?

A
  • Blood/Platelet transfusion
  • IV fluids
  • Allopurinol
  • Hickman/Subcut line - IV access
36
Q

Why would you give allopurinol to someone as supportive therapy for ALL?

A

To try to prevent tumour lysis syndrome

37
Q

What are characteristics of blast cells?

A

An immature precursor of myeloid cells or lymphoid cells:

  • Bigger than normal counterpart
  • Immature nucleus (nucleolus, open chromatin)
  • Cytoplasmic appearances often atypical
  • Rarely ever seen in serum of normal individuals

If present, are highly suggestive of an acute leukaemia or a chronic disorder that is beginning to transform into an acute disease

Gwen - Haematology (33 decks)

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