Leukaemia Flashcards

1
Q

Where does haematopoesis occur in the bone marrow?

A

in the red marrow

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2
Q

What is the pathogenesis of leukaemia?

A

mutations happen in the precursor cells that give them a survival advantage and they can hide from our immune system
these cells replicate unregulated and take over the bone marrow = clonal expansion of blast (immature cells) - these blasts cells should be in very small numbers in the bone marrow and not present at all in the peripheral blood, but in leukaemia, these cells fill the bone marrow and the blood
this results in bone marrow failure due to accumulation of blasts

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3
Q

What is the difference between the acute and chronic leukaemias?

A

the acute leukaemias come on very quickly and the problem is with the more immature cells eg stem cells (haemoblast) and common myeloid and common lymphoid progenitors
Chronic leukaemias come on slower and are a clonal expansion of the more mature cells

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4
Q

Which cells are affected in chronic myeloid leukaemia?

A

clonal expansion of basophils, neutrophils and eosinophils

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5
Q

Which cells are affected in chronic lymphocytic leukaemia?

A

mature lymphocytes eg B cells and T cells

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6
Q

Which cells are affected in acute lymphoblastic leukaemia?

A

lymphoblasts - the precursors of T and B cells

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7
Q

Which cells are affected in Acute myeloid leukaemia?

A

myeloblasts (the precursors of basophils, neutrophils, eosinophils and monocytes)

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8
Q

What are the risk factors for leukaemia?

A

Congenital eg germline mutations giving genetic predisposition
Down’s syndrome and AML
environmental: radiotherapy, chemo, benzene and other chemicals

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9
Q

What are the signs and symptoms of leukaemia?

A

anaemia: SOB, fatigue
thrombocytopenia: bruising, mucosal bleeding, rash - purpura and petechiae (non-blanching)
splenomegaly
infection: fevers/rigors
in leukaemia, these symptoms come on very quickly
infiltrations of the skin and other organs
gum hypertrophy
sometimes: SVCO, 3rd CN palsy

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10
Q

What investigations are done for leukaemia?

A

a) FBC
b) coagulation screen - present with coagulopathy eg in DIC + can bleed
c) biochem: U+E, LFT, Calcium, LDH, uric acid, B12, folate - to check liver and kidney function
d) group and screen
e) virology - HIV, Hep B, Hep C
f) CXR - as can get a large mediastinal mass
g) flow cytometry -to identify cell surface markers
h) cytogenetic analysis - identifies abnormal genetic changes and helps in prognosis
i) bone marrow biopsy -

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11
Q

What is the most common age range for ALL?

A

it is the commonest malignancy of childhood

median age is 3.5 years

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12
Q

What is the peak age of incidence of AML?

A

70 years old

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13
Q

What are the histological feature of myeloblasts?

A

Auer rods in the cytoplasm

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14
Q

Give examples of supportive means of treating a pt?

A

a) fluids
b) bone marrow support - blood and platelets
c) infection prevention and treatment: prophylactic antifungals, prophylactic antibiotics
d) treat the symptoms of treatment eg mucositis, diarrhoea, constipation, nausea, vomiting
e) pain relief
f) holistic care: psychological and emotional, relatives

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15
Q

What is the opposite of supportive treatment?

A

definitive treatment

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16
Q

Aspergillus is angioinvasive true or false?

A

true

17
Q

What does mucositis cause for the pt?

A

they get a sore mouth and they can’t eat or drink

18
Q

What is the aim of chemo?

A
  1. to bring pts to remission, by wiping out everything in the bone marrow with chemo +/- bone marrow transplant
  2. keep them in remission
19
Q

How long is chemo given for in leukaemia?

A

3 years for men

2 years for women

20
Q

Are acute leukaemias aggressive or indolent?

A

aggressive eg pts with AML don’t usually survive more than a year

21
Q

Which leukaemia is associated with the Philadelphia chromosome?

A

chromic myeloid leukaemia

22
Q

what is the philadelphia chromosome?

A

translocation of long arm of chromosome 22 and the long arm of chromosome 9

23
Q

How is the philadelphia chromosome detected?

A

karyotyping or FISH

24
Q

What is the first line treatment of CML?

A

Gleevec - a tyrosine kinase inhibitor, also known as imatinib