Haematological malignancies Flashcards by Jasmine Henson

Define lymphoma

haematological malignancies of lymphoid lineage (cancers of lymph nodes)

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Lymphoma presentation

(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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What are the B symptoms?

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

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Characteristics of high grade lymphomas

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

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Characteristics of low grade lymphomas

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

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How is lymphoma diagnosed?

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

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Describe Burkitt lymphoma

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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Describe Hodgkin lymphoma

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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What cells would be present in Hodgkin Lymphoma?

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

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Describe CLL

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

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Presentation of CLL

usually incidental lymphocytosis on FBC

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

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What is the diagnosis of lymphadenopathy and no lymphocytosis?

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

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How is a diagnosis of CLL made?

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

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When would you treat CLL?

bulk disease
disease obstructing major organ
bone marrow failure
B symptoms

if not, ‘watch + wait’

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CLL treatments

monoclonal antibody + chemotherapy
B-cell signalling inhibitors

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Describe CML

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

CML presentation

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

CML diagnosis

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

CML treatment

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

Acute leukaemia presentation

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

Acute leukaemia diagnosis

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

When are Auer rods seen?

AML

What age groups are AML and ALL seen in?

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

What subtype of AML is associated with DIC?

Acute promyelocytic leukaemia (APML)

AML/ALL treatment

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)

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

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

Benign neoplasm features

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

Malignant neoplasm features

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

Describe TNM classification

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

How are tumours of the haematopoietic and lymphoid tissues classified?

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

Define AML

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

What are the subtypes of Hodgkin Lymphoma?

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

List some Non-Hodgkin lymphoma subtypes

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

Why is it important that classification of neoplasms is standardised?

- accuracy of diagnosis, grading and staging - tailored treatment - comparison between series (therapy/outcome)

Causes of massive splenomegaly

Myelofibrosis CML Malaria

Splenomegaly signs/symptoms

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

Lymphadenopathy due to infection signs/symptoms

acute onset pain + swelling localised tender lymph nodes

Lymphadenopathy due to malignancy signs/symptoms

insidious onset painless generalised area affected