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Haematology > malignant haematology and acute leukaemia > Flashcards

malignant haematology and acute leukaemia Flashcards

1
Q

persistent, unexplained high lymphocyte count for years

A

low-grade lymphoproliferative disorder

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2
Q

what usually characterises malignant haemopoiesis

A

increased numbers of abnormal and dysfunctional cells
loss of normal activity

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3
Q

what are haematological malinancies due to (one or more of these)

A

increased proliferation (in absence of a stimulus)
lack of differentiation/maturation
lack of apoptosis

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4
Q

proliferation of abnormal progenitors with block in differentiation/maturation

A

acute myeloid leukaemia

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5
Q

proliferation of abnormal progenitors but NO differentiation/ maturation block

A

chronic myeloid leukaemia

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6
Q

classifications of haematological malignancies

A

based on lineage
based on developmental stage (precursor) within lineage
based on anatomical site involved

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7
Q

types of haematological malignancies based on lineage

A

myeloid
lympoid

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8
Q

haematological malignancy based on blood involvement

A

leukaemia

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9
Q

haematological malignancy based on lymph node involvement with lympoid malignancy

A

lymphoma

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10
Q

which haematological cancers are histologically and clinically more aggressive

A

acute leukaemia
high grade lymphomas

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11
Q

features of histological aggression

A

large cells with high nuclear-cytoplasmic ration, prominent nucleoli, rapid proliferation

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12
Q

features of clinical aggression of haematological cancers

A

rapid progression of symptoms

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13
Q

acute leukaemia

A

rapidly progressive clonal malignancy of the marrow/blood with maturation defects
defined as an excess of blasts in either the peripheral blood or bone marrow

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14
Q

types of acute leukaemia

A

acute myeloid leukaemia
acute lymphoblastic leukaemia

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15
Q

what is acute lymphoblastic leukaemia

A

malignant disease of primitive lympoid cells
most common childhood cancer

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16
Q

presentation of acute lymphoblastic leukaemia

A

due to marrow failure: anaemia, infections, bleeding
leukaemic effects: high count with obstruction of circulation, involvement of areas outside the marrow and blood (CNS, testes)
bone pain

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17
Q

what is acute myeloid leukaemia

A

more common in the elderly
may be de novo or secondary

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18
Q

presentation of AML

A

similar to ALL: marrow failure (anaemia, infections, bleeding)
subgroups have specific presentations: coagulation defect- DIC in acute promyelocytic
gum infiltration

19
Q

investigations for acute leukaemia

A
  • Blood count and film
  • Coagulation screen
  • Bone marrow aspirate
    • Morphology
    • Immunophenotype
    • Cyto/molecular genetics - diagnostic utility, prognostic significance
    • Trephine - enables better assessment of cellularity and is helpful when aspirate is sub-optimal
20
Q

what would you see on a blood film in acute leukaemia

A

reduction in normal
presence of abnormal
- blasts: high nuclear: cytoplasmic ration

21
Q

what would you expect to see in bone marrow in acute leukaemia

A

morphology: large cells, with high nucleus: cytoplasmic ration and prominent nucleoli
immunophenotyping: distuingish between myeloid and lymphoblastic
cyto/molecular genetics: diagnostic utility
trephine: enables better assessment of cellularity and helpful when aspirate sub-optimal

22
Q

treatment of ALL

A

can last up to 2-3 years
- different phases of treatment of varying intensity
- targeted treatments in certain subsets
- CNS directed treatment

23
Q

treatment of AML

A

between 2-4 cycles of chemotherapy
prolonged hospitalisation
targeted treatments in subsets
hickman line used

24
Q

complications of marrow suppression

A

anaemia
neutropenia
thrombocytopenia

25
Q

what is neutropenia

A

increased severity and duration of infections
gram negative bacteria can cause fulminant life-threatening sepsis in neutropenic patients
patients also susceptible to fungal infections

26
Q

what is thrombocytopenia presenting as

A

bleeding
- purpura
- petechiae

27
Q

complications of treatment for acute leukaemia

A

nausea and vomiting
hair loss
liver, renal dysfunction
tumour lysis syndrome (during first course of treatment)
infection

28
Q

what infections can be complications of chemo

A

bacterial: empirical treatment with broad spectrum ABx as soon as neutropenic fever
fungal: if prolonged neutropenia and persisting fever unresponsive to anti-bacterial agents
penumocystis jirovecci penumomnia

29
Q

what is chronic myeloid leukaemia

A

proliferation of myeloid cells- granulocytes and their precursors

30
Q

aetiology of chronic myeloid leukaemia

A

the philadelphia chromosome
- translocation of genes between chromosome 9 and 22
- results in a new gene- BCR-ABL1

31
Q

3 typical phases of CML

A

the chronic phase, the accelerated phase and the blast phase

32
Q

what is the chronic phase of CML

A

can last around 5 years
often asymptomatic and patients are diagnosed incidentally with raised white cell count

33
Q

what is the accelerated phase of CML

A

occurs where the abnormal blast cells take up a high proportion of the cells in the bone marrow and blood
- patients become symptomatic: anaemia, thrombocytopenia, immunocompromised

34
Q

what is the blast phase of CML

A

involves an even higher proportion of blast cells to the accelerated phase
severe symptoms and pancytopenia
often fatal

35
Q

presentation of CML

A

splenomegaly
hypermetabolic symptoms: night sweats, weight loss, gout, hyperuricemia, fever

36
Q

investigations for CML

A

bloods:
- FBC: normal/decreased HB, increased WBC, decreased platelets
- blood film: neutrophilia
- leukocyte alkaline phosphatase (LAP)- usually reduced
bone marrow biopsy: would show increased cellularity with increase granulocytes

37
Q

management of CML

A

fatal without stem cell/bone marrow transplant in the chronic phase
durable treatment response with tyrosine kinase inhibitors: imatinib

38
Q

what is chronic lymphocytic leukaemia

A

occurs where there is chronic proliferation of a single type of well differentiated lymphocyte: usually B-lymphocytes

39
Q

who gets CLL

A

usually adults over 55

40
Q

presentation of CLL

A

often asymptomatic
can present with infections, anaemia, bleeding and weight loss
can cause warm autoimmune haemolytic anaemia

41
Q

investigations for CLL

A

bloods:
- blood count: Hb normal/low, increased WCC, platelets normal/low
- blood film: increased lymphocytes (smear or smudge cells)
bone marrow:
- may be heavily infiltrated with lymphocytes
- immunophenotyping- mainly CD19/20 and CD5 B cells
- cytogenetic: deletion of 13 q

42
Q

coombs test in CLL

A

may be positive if there is haemolysis

43
Q

management of CLL

A

depends on the stage of the disease
- chemotherapeutic interventions in early stage disease is not usually necessary
- absolute indications for treatment include weight loss, night sweats, progressive marrow failure

44
Q

management of neutropenia and sepsis

A

piperacillin/tazobactam

Haematology (19 decks)

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