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ICC3 > introduction to haematological malignancies > Flashcards

introduction to haematological malignancies Flashcards

1
Q

what is the life span of RBC ?

A

120 days

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2
Q

what is the life span of platelets ?

A

10 days

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3
Q

what are the hematopoetic stem cells ?

A

lymphoid stem cells
pluripotent stem cells
myeloid stem cells

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4
Q

what to lymphoid stem cells give rise to ?

A

plasma cells/ B cells

T cells

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5
Q

what do pluripotent stem cells give rise to ?

A

lymphoid and myeloid stem cells

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6
Q

what do myeloid stem cells give rise to ?

A 
RBCs
Platelets
neutrophils 
monocytes 
eosinophils
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7
Q

what is the origin of haematological malignancies ?

A

they are of single cell origin

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8
Q

what are the features of acute leukemia ?

A

cells are blocked at an early stage of differentiation
rapidly growing
associated with early bone marrow failure

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9
Q

what are the symptoms of bone marrow failure ?

A

anemia
thrombocytopenia
neutropenia

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10
Q

what are the symptoms of tissue infiltration?

A

lymphadenopathy
gum hypertrophy
rash, subcutaneous chloromas
CNS infiltration

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11
Q

what is the clinical presentation of acute leukemia ?

A

splenomegaly
retinal haemorrhages
blast cells in blood film
gum hypertrophy

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12
Q

what is the treatment for acute leukemias?

A

stabilize the patient , treat any infections, stop bleeding, transfuse
start induction chemotherapy ( induction)
several courses of chemotherapy (maintenance)

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13
Q

how is prognosis decided in acute leukemia ?

A

based on response to induction chemotherapy and the presence of genetic alterations which activate particular oncogenes

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14
Q

what are the features of chronic leukemias ?

A

fully differentiated cells predominate
with accumulation of these mature cells
slower in growth
bone marrow failure is usually later in the disease

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15
Q

untreated chronic myeloid leukemia cases ?

A

progression to acute leukemia overtime

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16
Q

What is the common translocation in chronic myeloid leukemia (CML)?

A

9;22 Bcr:Abl fusion , Philadelphia chromosome

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17
Q

what does the hybrid protein created by Bcr;Abl fusion promote ?

A

increased proliferation , decreased apoptosis ( increased tyrosine kinase activity)

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18
Q

what is chronic lymphocytic leukemia

A

cancer of small b- lymphocytes associated with lymphocytosis (increased levels of WBCs)

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19
Q

where does CLL arise ?

A

arises in the bone marrow

20
Q

what are the clinical features of chronic lymphocytic leukemia ?

A

lymphocytosis with or without lymphadenopathy
hepatosplenomegaly
bone marrow failure

21
Q

what autoimmune diseases are associated with chronic lymphoid leukemia ?

A

immune thrombocytopenia , autoimmune haemolytic anemia

22
Q

what is the difference between a lymphoma and leukemia ?

A

lymphoma arises from lymphoid organs ( spleen and lymph nodes
leukemia arises from the bone marrow

23
Q

what are the clinical features of a lymphoma ?

A

lymph node enlargement
generally tired/unwell
weight loss
fever

24
Q

what is the management for lymphomas ?

A
  1. full staging investigations
  2. broad categorisation on histology to asses aggressiveness
  3. chemotherapy, radiotherapy and monoclonal antibodies
25
Q

how do non-hodgkin lymphomas arise ?

A

results from genetic events during antigen driven lymphocyte proliferation in peripheral lymphoid tissue

26
Q

where do high grade lymphomas arise from (Burkitts lymphoma) ?

A

dark zone in secondary lymphoid organs

27
Q

where do low grade lymphomas arise from ( follicular NHL)?

A

light zones in secondary lymphoid organs

28
Q

what is the genetic translocation that occurs in burkitts lymphoma ?

A

t(8;14) IgH Myc

29
Q

what is the genetic translocation that occurs in follicular NHL ?

A

t(14;18) IgH Bcl 2

30
Q

what are the positive finding sin a low grade follicular NHL in immunochemistry ?

A

CD20 poositivity

31
Q

what are the histological findings in hodgkin lymphoma ?

A

reed Sternberg cells

32
Q

what do myelomas rise from ?

A

plasma cells

33
Q

what is the common clinical presentation of multiple myelomas ?

A 
fatigue/anemia
bone pain/pathological fractures 
symptoms of hypercalcaemia 
symptoms of hyper viscosity 
renal failure
34
Q

what is the treatment for multiple myeloma ?

A

chemotherapy
steroids
targeted agents (protesome inhibitors, thalidomide and analogues )

35
Q

what are proteasome inhibitors ?

A

drugs that block the action of proteasome, cellular complexes that break down proteins

36
Q

what is serum protein electrophoresis ?

A

used to identify patients with multiple myeloma and other serum protein disorders

37
Q

what are the findings in SPEP in multiple myeloma patients ?

A

there will be a spike with gamma globulin proteins (M protein/myeloma protein)

38
Q

how is a laboratory diagnosis made for multiple myeloma ?

A

microscopy - blood, BM aspirate and trephine
immunophenotyping - flow cytometry
cytogenetics - FISH analysis
molecular genetics - PCR

39
Q

what are the typical antigens expressed by acute myeloid leukemia ?

A

CD33, 34, CD117, CD13 , cMPO

40
Q

what would you find in a bone marrow smear of a chronic lymphoid leukemia patient ?

A

smudge cells ( easily smudge lymphocytes)

41
Q

B cell CLL vs T cell CLL

A

95% are B cell lineages and T cell lineages have a worse prognosis

42
Q

what are the surface markers of B cells ?

A

CD19

43
Q

what is G banding ?

A

Giemsa banding is a technique used in cytogenetics to produce a visible karyotype by staining condensed chromosome

44
Q

what techniques are used to asses for minimal residual disease in AML ?

A

RT-PCR

45
Q

what is the genetic translocation in acute myeloid leukemia ?

A

t(15;17)

PML- RARA

ICC3 (66 decks)

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