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Yr5 Haematology > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

Who is affected by ALL?

A

Children

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2
Q

How common is ALL?

A

Most common malignancy of childhood

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3
Q

What genetic conditions can pre-dispose to leukaemia?

A

Down’s

Kleinfelter’s

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4
Q

Which virus can pre-dispose to leukaemia?

A

HLTV-1

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5
Q

What is the most common gene abnormality in leukaemia? What type of leukaemia does it usually cause?

A

Philadelphia Chromosome- Proto-oncogene
Abnormal Chr22- reciprocal translocation between Chr9 + Chr22
Associated w/97% cases of CML

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6
Q

Why does Myelodysplastic syndromes need monitoring?

A

Precursor to leukaemia

30% go on to AML

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7
Q

How is Myelodysplastic syndrome managed?

A

<5% blasts in BM: Conservative (RBC & Platelet transfusion), EPO
>5% blasts in BM: Supportive care (elderly), Chemo, BM transplant (if <50yo)

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8
Q

Who is usually affected by AML?

A

Middle aged/elderly

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9
Q

What are the risk factors for acute leukaemia?

A 
White
Males
Younger age
Radiation dose: Maternal X-ray when pregnant
Genetics: Down's
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10
Q

How does ALL usually present?

A 
RAPID onset BM failure:
Anaemia: Dyspnoea, pallor, lethargy
Thrombo: Bruising, purpura
Neutro: Infections 
Systemic: ↓weight, fever, malaise
Lymphadenopathy
BONE PAIN
SPLENOMEGALY
Testicular enlargement
Cranial nerve palsy
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11
Q

How does AML usually present?

A

Marrow failure (anaemia, thrombocytopenia, neutropenia)
Systemic: ↓weight, fever, malaise
Bone pain
Violaceous skin lesions

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12
Q

How is ALL investigated?

A
  • Blood Film: LYMPHOBLASTS
  • Bloods:↓Hb, ↓Plt ↓Neut,↑WBC (poor prog)
  • BM Aspirate: ↓erythropoiesis ↓megakaryocytes (plt precursors) > 20% blasts
  • Flow cytometry immunophenotyping: Tumour lineage (myeloid/lymphoid)
  • CXR: Mediastinal widening
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13
Q

How is AML investigated?

A
  • Blood Film: AUER RODS, myeloid blasts
  • Bloods: Bloods:↓Hb, ↓Plt ↓Neut,↑WBC (poor prog)
  • BM Aspirate: ↓erythropoiesis ↓megakaryocytes (plt precursors) > 20% blasts
  • Flow cytometry immunophenotyping: Tumour lineage (myeloid/lymphoid)
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14
Q

How are Auer rods visualised?

A

Blood film w/myeloperoxidase stain

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15
Q

How are ALL & AML differentiated between?

A 
Auer Rods: YES = AML, NO = ALL 
Lymphoblasts: YES = ALL, NO = AML
Bone &amp; joint involvement: YES = ALL, NO = AML
Hepatosplenomegaly: YES = ALL, NO = AML
Organ infiltration: YES = ALL, NO = AML
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16
Q

What is the prognosis of untreated & treated acute leukaemia?

A

Untreated: Fatal within months
Treated: Approx 1 year

17
Q

What are the treatment options for acute leukaemias?

A

Palliative

Curative intent

18
Q

What are the 3 phases of ‘curative’ treatment for acute leukaemia?

A

1) Remission induction: Majority of tumour destroyed by induction chemo= BM hypoplasia (ICU admission as ↓↓WCC)
2) Remission consolidation: wait until normal haematopoesis → 3-4week cycle of chemo to attack remaining tumour cells, may include BM transplant AIM TO ACHIEVE COMPLETE REMISSION
3) Maintaining remission: Outpatient Tx for >3yrs THEN if ALL observe

19
Q

What are the options for palliative care in acute leukaemia?

A

Supportive: Control bleeding, Tx Sx of anaemia (RBC transfusion), Tx infections (prophylactic Abx & antifungals)

20
Q

What is the major difference in the treatment of ALL & AML?

A

ALL patients w/ALL get CNS treatment

21
Q

What is the prognosis like in ALL?

A

Kids = Very good
Complete remission is obtained in almost all
80% alive at 5years

22
Q

What is a high risk complication of BM transplant in leukaemia patients?

A

Graft vs Host disease

23
Q

What is the pathophysiology of ALL?

A

↑No of Lymphoid Blast cells push other cells out of bone marrow acutely → rapid onset of Anaemic, Neutropenic, thrombocytopenic Sx

24
Q

What is a complication of ALL?

A

Tumour lysis syndrome → Renal failure

25
Q

Who is usually affected by CLL?

A

Elderly

26
Q

Which cells are usually affected in CLL?

A

B lymphocytes

27
Q

What cells are affected in CML

A

Affects the myeloid cells:

Basophils, neutrophils and eosinophils.

28
Q

What is the natural progression of CML?

A

Chronic phase → Aggressive phase → blast phase (>20% blast cells)

29
Q

What is a blast crisis?

A

Acute terminal phase of CML
Mortality↑↑↑
>20-30% blast cells in the blood or bone marrow

30
Q

What are the Sx of CML?

A 
SOB
Abdominal discomfort/splenic pain- splenomegaly
Fever &amp; Night sweats
Lymphadenopathy
Gout (↑cell turnover = ↑urate)
Dyspnoea &amp; cough
31
Q

What are the Sx of a blast crisis?

A 
Rapid increase in proportion of blast cells
Fever
Bone pain
Fatigue
Splenomegaly
Sx of anaemia
Sx of thrombocytopenia
32
Q

What investigations are done for suspected CML?

A

Bloods: ↑WBC, Hb↓/n
Blood Film: Neutrophilia w/myeloid precursors, LARGE white cells
BM Aspirate: ↑↑no. of cells
FISH: Find Philadelphia Chromosome

33
Q

How is CML managed?

A

Imatinib (stops BCR-ABL fusion)- continued indefinitely if needed. If used in aggressive disease → chronic disease
Stem cell transplantation
Autologous transplant

34
Q

How is CLL present?

A

Usually asymptomatic (incidental finding)
Immunosuppression: Recurrent infections, anaemia
Painless lymphadenopathy
Splenic pain
Hepatomegaly / splenomegaly++

35
Q

How is CLL investigated?

A

Blood: ↑↑WCC, Hb↓/n
Blood Film: ↑lymphocytes, Smudge/Smear cells
BM Aspirate: Similar to peripheral blood
Cytogenetics

36
Q

How is CLL managed?

A

Chlorambucil +/- Prednisolone

Chemo

Yr5 Haematology (6 decks)

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