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Haematology > Haematology 1 - Acute leukaemia > Flashcards

Haematology 1 - Acute leukaemia Flashcards

1
Q

Which cells are affected in the different leukaemias?

A

AML- can affect ay of the cells in the myeloid lineage

CML- affects pluripotent haemoatopoietic stem cell

  • In chronic phase, it is characterised by overproduction of myelocytes
  • In acute phase, they can undergo a lymphoblastic transformation (lymphoblastic crisis)

ALL- affects mature T cells or B cells

CLL- affects mature B cells (*T cell is uncommon)

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2
Q

What is the median age of presentation of AML?

A

65-70

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3
Q

what are the two types of mutation that result in AML?

A

Type 1: promotes proliferation and survival eg FLT3-ITD

Type 2: blocks differetiation (differentiation is good, and usually followed by apoptosis) eg PML-RARA

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4
Q

Recall some genetic associations of AML

A

a) translocation: t(15;17) >>> PML-RARA fusion gene >>> APML

b) inversion of chromosome 16
c) trisomies/duplications

  • Trisomy 21- Downs or Trisomy 8
    d) deletions
  • 5q deletion
  • 7q deletion
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5
Q

Which chromosome abberation causes APML?

WHat are the type 1 and type 2 mutations that cause APML?

A

Type 1 mutation: FLT3-ITD

Type 2:

  • t(15,17)
  • Fusion of PML-RARA
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6
Q

Which type of leukaemia is most likely to cause haemorrhage?

A

Acute Promyelocytic leukaemia (APML)

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7
Q

Which type of leukaemia is most likely to cause DIC + hyperactive fibrinolysis

and what would you see in clotting studies

A

APML

  • Prolonged PT
  • Prolonged/short APTT
  • Low fibrinogen
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8
Q

What is the key triad of clinical features of AML + ALL

A

Anaemia
Thrombocytopaenia
Neutropaenia - although high WCC on FBC due to increase of blast cells

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9
Q

How can myeloid lineage be proved on blood film?

A

Presence of auer rods

*but if you don’t see auer rods you can’t be sure whether its myeloid or lymphoid

hence will need to do further tests

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10
Q

Recall some useful supportive therapies for AML+ ALL

A

Blood products: red cells, platelets and FFP
Antibiotics: PCP prophylaxis, broad-spec for fever
Long line
Allopurinol (as uric acid may be released from dying cells when treatment is started)

FLuid and electrolytes

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11
Q

Which type of leukaemia is most likely to present with long bone pain?

A

ALL

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12
Q

Recall some sites of leukaemic involvement in ALL that you wouldnt see in AML

A

Thymus, testes, CNS, bone pain

lymphadenopathy- less common in AML

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13
Q

Which ALL patients are appropriate for imatinib treatment?

A

Philadelphia chromosome positive

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14
Q

What is the best technique to differentiate between AML and ALL?

A

Immunophenotyping

  • immunocytochemistry
  • immunohistochemistry

This has replaced cytochemistry ((Myeloperoxidase, Sudan Black, Non-specific Esterase) etc..

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15
Q

What is aleukaemic leukaemia?

A

type of AML

When the leukaemic cells are not in the peripheral blood, they are restricted to the bone marrow

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16
Q

Targeted treatment for AML

A

ATRA for APML

  • Supportive
    • RBCs, platelets, FFP/ cryo if DIC, Abx, central line, allopurinol, fluids
  • Combination chemotherapy
    • 4-5 courses (2 x induction, 2-3 x consolidation)
    • Treatment= 6 months
  • Molecular targeted therapy
    • Tyrosine kinase inhibitors- Imatinib (if Ph chromosome +ve)
    • Antibody treatment- gemtuzumab ozogamicin (CD33mAb-cytotoxic antibiotic)
  • Transplantation if poor prognosis
17
Q

Epidemiology of ALL vs AML

A

ALL- commonest in children

  • Second peak in elderly (50-60 years) >>>Philadelphia chromosome +ve

AML- adults,

Neonates: often (30%) develop transient abnormal myelopoeisis; resembles AML but resolves spontaneously and completely after few weeks

18
Q

Clinical features of ALL vs AML

A

ALL-

  • triad- anaemia, thrombocytopaenia, neutropenia
  • lymphadenoapthy
  • hepatosplenomegaly
  • extramedullary disease is more common eg CNS infiltration
  • Testicular enlargement
  • Thymic enlargement - mediastinal mass esp T cell ALL
  • bone pain

AML

  • triad- anaemia, thrombocytopaenia, neutropenia
  • lymphadenopathy is less common
  • specific subtypes:
    • APML can present with DIC
    • monocytic subtype can present with gum (And skin) infiltration (Monocytic in MOUTH) + hypokalaemia
19
Q

Investigations findings for AML vs ALL

A

ALL:

  • high WCC- blasts (>20%)
  • blasts often have blebs/tails of cytoplasm
  • immunophenotyping via flow cytometry - important to confirm diagnosis
    • CD34- precursor stem cells
    • CD 3, 4, 8 - T lymphocytes
    • CD19, CD23, CD20 - B cells

AML:

  • high WCC- blasts (20%)
  • auer rods + granules - may be present - but not always
  • immunophenotyping via flow cytometry
    • CD34 - precursor stem cells
    • CD 33, CD 13, MPO (myeloid cells)
20
Q

Treatment of AML vs ALL

A

ALL:

  • chemotherapy
    • remission induction - chemo agents often given with steoids
    • consolidation- high dose multi drug chemotherapy
    • CNS treatment if indicated
    • maintenance- 2 years in girls and adults, 3 years in boys
    • Boys treated for longer because testes are a site of accumulation of lymphoblasts
  • consider allogeneic stem cell transplant if high risk of relapse

AML

  • Chemotherapy
    • Remission induction: daunorubicin, cytarabine
  • Consolidation: cytarabine
  • No CNS prophylaxis/maintenance therapy needed usually
  • Allogeneic stem cell transplant- consider if high risk of relaps e
  • Targeted treatment
    • ATRA for APML
    • Midostaurin- FLT3 mutations
    • Gemtuzumab- CD33 immunotherapy
    • Enasidenib- IDH mutations
  • Supportive treatment
    • blood products
    • Abx
    • Allopurinol
    • Fluid
    • Electrolytes

**NB- supportive involves prevention of Tumour Lysis syndrome: FBC may show ‘tumour lysis syndrome’ = high K+, LDH, PO42-, uric acid

21
Q

Which haematological malignancies can be philadelphia positive?

A

CML and some ALL

(ALL- tends to be in the second peak that occurs in the elderly)

Chr 9,22 translocation

22
Q

ACUTE leukaemia =

A

>20% blasts present

23
Q

what determins good prognosis for ALL

A
  • Cytogenetics
    • Good prognosis:
      • Hyperdiploidy
      • t(12;21)
      • t(1;19)
  • Bad prognosis:
    • t(4;11)
    • Hypodiploidy
  • Bad prognosis of ALL in kids= VERY high WCC
  • NOTE: non-Caucasian and males are also poor prognostic factors
24
Q

cytogenetics of AML

A
  • Cytogenetics:
    • t(8;21)
    • Inversion on Chr 16
25
Q

treatment for APML and is acute promyelocytic leukaemia curable

A
  • CURABLE – 90% 5-year survival
  • Treatment: Platelets, chemotherapy, All-trans-retinoic acid (ATRA), A2O3
26
Q

what is tumour lysis syndrome + how is treated

A

FBC may show ‘tumour lysis syndrome’ = high K+, LDH, PO42-, uric acid

supportive therapy:

Fluids + electrolytes + allopurinol

  • IMMEDIATE action high WCC >>> reduce Tumour Lysis Syndrome: Allopurinol + hyperhydration

Haematology (16 decks)

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