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Haematology > Haematological Malignancies > Flashcards

Haematological Malignancies Flashcards

1
Q

What is leukaemia?

A

Leukaemia cells in bone marrow

Circulate in peripheral blood

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2
Q

What is Myelodysplasia?

A

Insufficient production of mature blood cells +/- leukaemia in the peripheral blood/bone marrow

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3
Q

What are myeloproliferative disorders?

A

Excessive production of mature blood cells

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4
Q

What are lymphomas?

A

Lymphoid cancers in lymphoid containing tissues

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5
Q

What are plasma cell dyscrasias?

A

Increased plasma cells in the bone marrow

Increased plasma cells –> paraprotein formation –> end organ damage

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6
Q

Effects of blood cancers on the body?

A

Formation of cancerous cells
Loss of production of other blood cell lines
Hepatosplenomegaly
Lymphadenopathy –> compressive symptoms
Orthopaedic complications - fractures, bone pain
Neurologic complications
Metabolic complications - calcium and urate

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7
Q

Viruses associated with haematological malignancies?

A

EBV

  • -> Hodgkins lymphoma
  • -> Burkitt lymphoma
  • -> Post-transplant lymphporliferative disorder

HTLV-1
–> Acute T lymphoblastic leukaemia/lymphoma

HIV

  • -> Cerebral Diffuse Large B Cell Lymphoma
  • -> Hodgkin lymphoma
  • -> Diffuse large B cell lymphoma

HHV-6
–> Primary effusion lymphoma

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8
Q

Environmental exposures associated with haematological malignancies

A

Chemotherapy - etoposide, anthracyclines, ASCT

  • -> AML
  • ->MDS

Radiation

  • -> AML
  • -> CML
  • -> Mylodysplasia

Benzene exposure
–> Multiple myeloma

Hair dye
–> follicular lymphoma

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9
Q

Familial haematological malignancies

A

Li Fraumeni - p53

Bloom syndrome - BLM gene

Runx1 –> acute leukaemia

GATA2 –> myelodysplasia

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10
Q

Diagnosis of AML

A

Blood film:

  • Acute = >20% blasts
  • Myeloid = Auer rods

Cytochemistry:
- Myeloid = myeloperoxidase positive

Immunophenotyping
- Myeloid antigens

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11
Q

Poor prognostic factors for AML

A

Age >60yrs

Cytogenetics:

  • t(9:22)
  • Del7, del5q, inv(3)
  • Complex cyogenetics >2 abnormalities
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12
Q

Good prognostic factors for AML

A

Cytogenetics:

  • t (15:17) = APML
  • inv (16)
  • t (8:21)
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13
Q

What if AML cells carry a normal genotype?

A

Molecular markers

Poor prognosis = Flt3 positive

Good prognosis = Flt3 negative and NPM1 positive

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14
Q

Treatment of AML

A

Prognostic factors at diagnosis = treatment strategy

If good health = chemotherapy –> Allogenic BMT
If poor health = supportive care

Relapse = Allogenic BMT or trials

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15
Q

Diagnosis of ALL

A

Blood film:

  • Acute =>20% blasts
  • Lymphoblastic = no auer rods

Immunophenotyping:
- B cell or T cell

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16
Q

Poor prognostic factors for ALL

A

Paediatric = 11q23 MLL translocations

Adult:
= T (9:22)
= Bcr-Abl

Minimal residual disease post chemotherapy

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17
Q

Good prognostic factors for ALL

A

Pediatric age group

18
Q

Treatment of ALL

A

Induction chemotherapy –>
Maintenance chemotherapy

Allogenic BMT

If Bcr-Abl –> Bcr-Abl inhibitor - imatinib, dasatinib

Immunotherapies

19
Q

Limitations of Allogenic BMT

A

Appropriate donor
Suitable recipient for transplant

Acute graft vs host disease
Chronic graft vs host disease

Infections
Treatment toxicity

Relapse post transplant

20
Q

Immunotherapies for ALL

A

CD20 positive = Rituximab

T cell mediated:

  • CD19/CD3 = Blinotumomab
  • Chimeric antigen receptor modified T cell infusions
21
Q

Diagnosis pf CLL

A

Lymphadenopathy

Blood film:

  • Many mature lymphocytes on peripheral BF
  • Smear cells
  • Haemolysis –> spherocytes
  • Thrmbocytopenia
  • BM faliure

Immunophenotyping:
- Lymphocytes kappa or lamba light chain restricted

22
Q

Clinical stages of CLL

A 
1 = Lymphocytosis only
2 = Lymphadenopathy
3 = Cytopenias
1+2 = observe only
3 = Treat if symptoms
23
Q

Prognosis of CLL

A

Poor:
11q and 17p deletions
Unmutated IgVH genes
ZAP-70 expression - associated with unmutated IgVH

Good:
13q deletion

24
Q

Treatment of CLL

A

Observe asymptomatic patients

Chemotherapy - oral or IV

p53 mutated = Alemtuzumab - OFF MARKET

Allogenic SCT

Trials

Can transform into ALL

25
Q

Diagnosis of Myelodysplasia

A

Bone marrow failure - anaemia + neutropenia +/- thrombocytopenia

+/- <20% blasts in the peripheral blood/BM

Risk of transformation to AML

26
Q

Classifications of Myelodysplasia

A
  1. Refractory anaemia
  2. 5q syndrome
  3. CML - PB monocytes >1
  4. MDS unclassified
27
Q

Why is 5q syndrome different?

A

5q deletion only

Females

Better prognosis

Treatment = lenolidomide

28
Q

Treatment of myelodysplasia

A

Supportive
- transfusions and iron chelation

Chemotherapy for CML

Allogenic SCT

29
Q

Classifications of Lymphoma

A

Hodgkins Lymphoma and Non-Hodgkins Lymphoma

Indolent NHL
- Marginal zone
- Follicular
TREAT ONLY IF SYMPTOMS

Aggressive NHL
- Diffuse large B cell lymphoma
- Burkitt Lymphoma
TREAT - RCHOP chemo +/-radio OR ASCT

30
Q

Hodgkins Lymphoma

A

Reed sternberg cells on histology

Prognosis and treatment based on Ann arbor staging

Chemotherapy and targeted radiotherapy

Relapse/refractory = Autologous SCT
Anti-CD30 Ab - brentuximab
PD-1 inhibitors

31
Q

Types of myeloproliferative disorders

A

CML

  • Neutrophilia +/- basophilia
  • Bcr-ABL postive

Polycythaemia Rubra Vera

  • High RBC mass
  • Headaches and erythromelalgia

Essential Thrombocytosis

  • Elevated platelets
  • Clots and vascular disease

Myelofibrosis

  • low counts
  • Leukoerythoblastic film
32
Q

Gene mutations in MPN

A

CML = Bcr-Abl
= Treatment with imatinib, nilotinib or dasatinib

PV and ET and MF = JAK2 V617F

If JAK2 negative ET and MF = Calreticulin positive
Good prognosis

33
Q

Treatment of PCV and ET

A

Thrombosis –> mortality and morbidity

Hydrea
Aspirin
Venesection
Interferon alfa or chlorambucil

34
Q

Treatment of myelofibrosis

A

Supportive:

  • Transfusion
  • Palliative chemotherapy
  • Splenectomy

Allogenic SCT

JAK1/2 inhibitor - Ruxolitinib - doesn’t improve survival

35
Q

Multiple Myeloma

A

> 10% malignant plasma cells on bone marrow
Monoclonal Ig in serum or urine - IgG>IgA>IgM>IgD

Treat if organ involvement - CRAB

Treatment :

  • Chemotherapy
  • Lenolidomide
  • Bortezomib - proteosome inhibitors
  • Autologous SCT
  • Radiotherapy for bone lesions
  • Bisphosophonates for bone lesions
36
Q

Primary systemic amyloidosis

A

MGUS with attitude
Amyloidogenic monoclonal protein
Elevated serum free light chains

Organ involvement - kidneys, heart, GIT, skin

Treatment same as MM

37
Q

Mechanism of action of ibrutinib?

A

Bruton’s tyrosine kinase inhibitor

Used to treat B cell cancers - mantle cell lymphoma, chronic lymphocytic leukemia, and Waldenström’s macroglobulinemia - NHL

38
Q

Mechanism of action of Idelalisib?

A

Phosphoinositide-3-kinase inhibitor

Used in combination with rituximab for relapsed CLL with p53 mutations

39
Q

Mechanism of action of ruxolitinib?

A

JAK-2 kinase inhibitor

PRV, ET and myelofibrosis treatment
No mortality impact but reduces symtpoms

40
Q

Mechanism of action of venetoclax?

A

BCL-2 homology region 3/BH3 mimetic

For CLL with 17p deletion

Haematology (7 decks)

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