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haematology > Haematological malignancies > Flashcards

Haematological malignancies Flashcards

1
Q

Define lymphoma

A

haematological malignancies of lymphoid lineage (cancers of lymph nodes)

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2
Q

Lymphoma presentation

A

(painless) swelling(s)
+/- B symptoms
splenomegaly
symptoms related to cytopenias (eg. anaemia, infections)
symptoms related to lumps in/compressing important structures
pruritis (normally Hodgkin’s)

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3
Q

What are the B symptoms?

A

night sweats (drenching)
fevers (unexplained)
weight loss (unintentional, 10% in 6 months)

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4
Q

Characteristics of high grade lymphomas

A

short history
grows quickly
patient usually symptomatic
treatment always required immediately
potentially curable
treatment = intensive chemotherapy

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5
Q

Characteristics of low grade lymphomas

A

longer or ‘no’ history
grows slowly
often asymptomatic
treatment often not required (watch + wait)
lifelong illness
treatment = less intensive chemotherapy

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6
Q

How is lymphoma diagnosed?

A

biopsy of lump
- core biopsy or whole node excision
- NOT fine needle aspirate (FNA)

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7
Q

Describe Burkitt lymphoma

A

subtype high grade lymphoma
very rapidly growing subtype of high grade B-cell non-Hodgkin lymphoma
t(8;14)
Endemic Burkitt Lymphoma associated with EBV infection

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8
Q

Describe Hodgkin lymphoma

A

high grade lymphoma
young adults + >60s
males>females
mediastinal mass common
associated with EBV
lymph node pain when drinking alcohol
good prognosis

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9
Q

What cells would be present in Hodgkin Lymphoma?

A

Reed-Sternberg cells (large, abnormal lymphocytes >1 nucleus)

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10
Q

Describe CLL

A

chronic lymphocytic leukaemia
mature lymphocytes
>70
normally slowly progressive treat only if symptomatic
no cure

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11
Q

Presentation of CLL

A

usually incidental lymphocytosis on FBC

may have:
- lymphadenopathy +/- splenomegaly
- marrow failure symptoms (anaemia/thrombocytopenia)
- B symptoms

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12
Q

What is the diagnosis of lymphadenopathy and no lymphocytosis?

A

small lymphocytic leukaemia (SLL)
- low grade non-Hodgkin’s lymphoma

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13
Q

How is a diagnosis of CLL made?

A

FBC (lymphocytosis)
blood film (smear/smudge cells)
Immunophenotyping for confirmation

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14
Q

When would you treat CLL?

A

bulk disease
disease obstructing major organ
bone marrow failure
B symptoms

if not, ‘watch + wait’

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15
Q

CLL treatments

A

monoclonal antibody + chemotherapy
B-cell signalling inhibitors

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16
Q

Describe CML

A

chronic myeloid leukaemia
less common than CML
caused by Philadelphia chromosome, t(9;22)
codes for new protein, BCR-ABL, a tyrosine kinase
always treated when diagnoses
can progress to AML

17
Q

CML presentation

A

may be incidental finding of neutrophilia with granulocyte precursors on FBC
symptoms related to anaemia
symptoms related to splenomegaly
B symptoms

18
Q

CML diagnosis

A

FBC
confirm with FISH (fluorescent in-situ hybridisation) to look for philadelphia chromosome (t(9;22))
bone marrow biopsy to assess phase

19
Q

CML treatment

A

tyrosine kinase inhibitor (eg. Imatinib)
daily tablets for rest of lives
aim for very low levels of BCR-ABL detected using PCR of blood

20
Q

Acute leukaemia presentation

A

consequences of cytopenias (bleeding, infections, anaemia)
short history –> quick treatment needed
can be very sick

21
Q

Acute leukaemia diagnosis

A

blasts on blood film/bone marrow (>20%)
immunophenotyping to confirm diagnosis (distinguishes AML from ALL)

22
Q

When are Auer rods seen?

A

AML

23
Q

What age groups are AML and ALL seen in?

A

ALL = children (little people)
AML = adults/elderly (mature people)

24
Q

What subtype of AML is associated with DIC?

A

Acute promyelocytic leukaemia (APML)

25
Q

AML/ALL treatment

A

intensive chemotherapy (chance of cure, very toxic)
may involve allogenic stem cell transplant

low intensity chemotherapy (may prolong life but not curative)

palliative care (symptom control)

26
Q

What else is often given alongside chemotherapy in AML/ALL patients?

A

Hickman line
prophylactic anti-microbials
transfusions (red cells, platelets)
treatment of neutropenic sepsis
pain control
anti-emetics
psychological support

27
Q

Benign neoplasm features

A

generally encapsulated
non-invasive
highly differentiated
few mitotic features
slow growth
little anaplasia (cells look the same)
non-metastatic

28
Q

Malignant neoplasm features

A

non-encapsulated
invasive
poorly differentiated
mitotic features common
can have rapid growth
relatively anaplastic (cells look different)
metastatic (or capable of becoming so)

29
Q

Describe TNM classification

A

T = tumour (size of primary tumour)
N = nodal involvement
M = distant mets

30
Q

How are tumours of the haematopoietic and lymphoid tissues classified?

A

by lineage:
- myeloid
- lymphoid
- histiocytic/dendritic cell
- mast cell

31
Q

Define AML

A

clonal expansion of myeloid blasts in the peripheral blood, bone marrow or other tissues

32
Q

What are the subtypes of Hodgkin Lymphoma?

A

Nodular lymphocyte predominant (popcorn cells on eosinophil background)
Classic Hodgkin lymphoma:
- nodular sclerosis
- lymphocyte-rich classical
- mixed cellularity classical
- lymphocyte-depleted classical

33
Q

List some Non-Hodgkin lymphoma subtypes

A

follicular lymphoma
diffuse large B-cell lymphoma
extra-nodal marginal zone lymphoma of MALT (MALT lymphoma)

34
Q

Why is it important that classification of neoplasms is standardised?

A
  • accuracy of diagnosis, grading and staging
  • tailored treatment
  • comparison between series (therapy/outcome)
35
Q

Causes of massive splenomegaly

A

Myelofibrosis
CML
Malaria

36
Q

Splenomegaly signs/symptoms

A

often asymptomatic
palpable splenic edge
pain in left upper abdomen that can radiate to left shoulder
feeling full without eating
frequent infections
bleeding easily

37
Q

Lymphadenopathy due to infection signs/symptoms

A

acute onset
pain + swelling localised
tender lymph nodes

38
Q

Lymphadenopathy due to malignancy signs/symptoms

A

insidious onset
painless
generalised area affected

haematology (16 decks)

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