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HAEMOTOLOGY > MedEd Lecture 1 > Flashcards

MedEd Lecture 1 Flashcards

1
Q

From which cell does acute/chronic myeloid leukaemia originate from?

A

common myeloid progenitor or multipotential haematopoietic stem cell

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2
Q

From which cell does acute lymphoblastic leukaemia originate from?

A

common lymphoid progenitor

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3
Q

From which cells does chronic lymphoblastic leukaemia originate from?

A

small lymphocyte, T lymphocytes or B lymphocytes

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4
Q

What is the outcome of acute leukaemias?

A

rapid proliferation of malignant cells resulting in bone marrow failure - stops producing normal cells

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5
Q

What are the clinical manifestations of acute leukaemias?

A

anaemia, thrombocytopenia, leukopenia/neutropenia

  • bone pain
  • usually generally unwell or septic
  • less common is spelnomegaly due to acute onset
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6
Q

What are the clinical manifestations of chronic leukaemias?

A

slower proliferation of malignant cells

  • bone marrow can still produce normal cells at the start
  • clonal cells can pool in lymph nodes or in the spleen
  • lymphadenopathy and splenomegaly
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7
Q

Typical history for Acute lymphoblastic leukaemia

A
  • 2-5 year old child
  • hepatosplenomegaly
  • bone pain / limp
  • fevers
  • CNS symptoms
  • testicular swelling (rare but specific - due to pooling of the cells)
  • in adults it’s similar to AML but you get lymphadenopathy or thymic masses
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8
Q

Acute lymphoblastic leukaemia typical bloods

A

neutropenia, thrombocytopenia, anaemia

  • may have high white cell count
  • circulating blasts in blood (this is variable depending on progression - higher in marrow at start then blood later on)
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9
Q

What does Acute Lymphoblastic look like on a blood film?

A

High nucelus:cytoplasm ratio

Nucelus looks more ‘open’ - paler purple/pink

May have nucleoli which look like small white punched out areas

‘Hand mirrors’

  • usually impossible to distinguish ALL from AML on film
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10
Q

How is Acute Lymphoblastic usually diagnosed?

A

Bone marrow and flow cytometry

  • Shows TdT+
  • CD19/CD22 B cells
  • CD2/CD3/CD4/8 T cells
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11
Q

What mutation is associated with 20-30% of Acute lymphoblastic leukaemia in adults?

A

BCR-ABL1 t(9;22) (philadelphia chromosome)

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12
Q

How is acute lymphoblastic leukaemia managed?

A

Chemo until remission or transplant

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13
Q

Typical patient with Acute Myeloid leukaemia

A
  • older patients (unusual in kids)
  • pre-existing myelodysplastic syndrome
  • symptoms of cytopenias
  • come in with sepsis
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14
Q

Blood tests of patient with acute myeloid leukaemia

A

anaemia
leukocytosis
thrombocytopenia
neutropenia
lots of blast cells
- normal INR, abnormal could be due to DIC due to acute promyelotic leukaemia

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15
Q

What is acute promyelotic leukaemia and how is it treated

A

associated with Acute myeloid and is when you get DIC

  • come in with big bleeds as well
  • good prognosis if treated early
  • give All-Trans Retinoid Acid (forces the cells to differentiate, stops proliferation)
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16
Q

Acute myeloid leukoaemia on blood film

A
  • auer rods (one is enough to diagnose)
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17
Q

How would you diagnose Acute myeloid leukaemia?

A
  • look for auer rods
  • if none then flow cytometry:
    MPO and CD13/33 are expressed
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18
Q

What translocation is associated with acute promyelotic leukaemia?

A

T(15;17)

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19
Q

How is acute myeloid leukaemia treated?

A

chemo

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20
Q

What are myeloproliferative neoplasms?

A

when you’re making too much of the cells of the myeloid lineage

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21
Q

What is essential thrombocythaemia?

A

Making too many platelets

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22
Q

How many platelets in essential thrombocythaemia?

A

over 450 times 10 to the 9

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23
Q

What mutation is associated with essential thrombocythaemia?

A

JAK2 (55% of cases)

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24
Q

How is essential thrombocythaemia treated?

A
  • aspirin to reduce stroke risk
  • hydroxycarbamaide lowers the count
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25
Q

What is the haematocrit in polycythaemia vera?

A

over 0.52 in men over 0.48 in women

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26
Q

Complications of polycythaemia vera

A

You also get thrombocythaemia so high risk of thrombotic events

  • can become myelofibrosis
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27
Q

Mutation for polycythaemia vera

A

JAK2 (95%)

28
Q

Treatment for polycythaemia vera

A

aspirin for stroke risk
- venesection to lower haematocrit
- hydroxycarbamide to lower count

29
Q

What is myelofibrosis?

A

clonal proliferation of stem cells in the bone marrow resulting in cytokine release and fibrosis of the bone marrow

  • therefore reduced production of all cell lineages due to the fibrosis
30
Q

Associations with myelofibrosis

A

JAK2 (50%)
Pancytopenia
Splenomegaly (massive)

31
Q

Management of myelofibrosis

A
  • stem cell transplant
  • Ruloxitnib - JAK inhibitor
32
Q

What happens in Chronic myeloid leukaemia?

A

overproduction of myeloid lineage (so it’s a type of myeloproliferative neoplasm)

33
Q

Typical presentation of chronic myeloid leukaemia

A

35-55 age

LUQ pain - splenomegaly

Usually asymptomatic during chronic phase

  • May present with symptoms of acute leukaemia in the accelerated/blast phase
34
Q

Bloods in chronic myeloid leukaemia

A
  • leukocytosis
  • neutrophilia
  • platelets high initially
  • low monocytes
  • high basophils
35
Q

Blood film in chronic myeloid leukaemia

A

’ left shift ‘
leukocytosis
eosinophilia
basophilia

36
Q

What chromosome is Chronic myeloid leukaemia associated with?

A

Philadelphia = BCR-ABL1 due to t(9;22)

37
Q

What are the phases of chronic myeloid leukaemia?

A

Chronic

Accelerated (increasing blasts, lack of response to therapy)

Blast phase (over 20% of bone marrow cells are blasts, behaves like an acute leukaemia)

38
Q

How is chronic myeloid leukaemia treated?

A

Tyrosine kinase inhibitor
1 = Imatinib

over 90% 10 year survival

39
Q

Chronic lymphoblastic leukaemia presentation

A
  • usually asymptomatic
  • picked up on routine bloods
  • usually over 50 with increasing incidence with age
  • more common in men
  • lymphadenopathy/splenomegaly
  • can present with ITP/haemolytic anaemia
40
Q

Blood and blood film for chronic lymphoblastic leukaemia

A

normal except raised white cell count (predominantly mature lymphocytes)

smear/smudge cells

41
Q

How is chronic lymphoblastic leukaemia diagnosed?

A
  • smear/smudge cells
  • flow cytometry = ‘ clonal ‘ population of cells will express same cell markers (one of kappa or lambda light chains), generally B cell markers
42
Q

How is chronic lymphoblastic leukaemia treated?

A

Stage A = no cytopenia, <3 areas of lymphoid involvement = watch and wait

Stage B = no cytopenia, 3+ areas of lymphoid involvement = consider treatement

Stage C = cytopenia = treat (targeted drugs)

43
Q

What is Richters syndrome?

A

when CLL transforms into an aggressive acute leukaemia

44
Q

What are myelodysplastic syndromes?

A

dysplastic changes (abnormal) to one or more myeloid cell lines (erythroid, megakaryocyte, granulocyte)

  • usually asymptomatic but can progress to AML
  • incidental cytopenia
45
Q

Summary of difference between Hodgkins and Non-Hodgkins

A

Hodgkins = young, mediastinum pymph nodes, agressive, mostly curable

Non-Hodgkins = older, lymph nodes anywhere, variable course and varibale curability

46
Q

Staging of lymphoma

A

Ann-Arbor staging

Stage 1 = Nodes affected on one group
Stage 2 = More than one group but on same side of diaphragm
Stage 3 = Gone to both sides of diaphragm
Stage 4 = bone marrow/spleen involvement

47
Q

B Symptoms of lymphoma

A

fever over 38
drenching night sweats
unintentional weight loss over 10% in past 6 months

48
Q

Hodgkin’s summary

A

young people
B symptoms
mediastinal lymphadenopathy
Redd-Sternburg cells are diagnostic (2 nuclei)
associated with EBV
treatment is chemo + radio

49
Q

Non-Hodgkin’s summary

A

lots of types
usually B cell
B symptoms or lymphadenopathy
incidence increases with age

50
Q

Examples of indolent non-hodgkin’s lymphoma

A

Follicular lymphoma
Small lymphocytic lymphoma

51
Q

Follicular lymphoma genetics and diagnosis

A

t(14;18) causes fusion of BCL2 gene
centroblasts on lymph node biopsy

52
Q

Follicular lymphoma treatment

A

watch and wait unless high burden of disease

53
Q

Example of a high-grade non-hodgkin’s

A

diffuse large B-cell lymphoma

54
Q

Risk of what with diffuse large B cell lymphoma treatment and Burkitt’s lymphoma

A

tumour lysis syndrome

55
Q

What is mantle cell lymphoma?

A

t(11;14) causes overexpression of cyclin D1

  • treat with chemo
56
Q

Example of very high grade lymphoma

A

Burkitt’s

57
Q

Associations, genetics and presentation of Burkitt’s

A

’ starry sky’ on histology
associated with t(8;14)
- associated with EBV and HIV
- large, fast growing lymph nodes in neck and elsewhere

58
Q

Give an example of a T cell lymphoma and its associations

A

Adult T cell lymphoma
- HTLV-1 common in Japan
- ‘ flower cells’ on blood film

59
Q

What is multiple myeloma?

A

clonal population of plasma cells which proliferate and produce monoclonal immunoglobulin light chains

60
Q

Key diagnosis findings for multiple myeloma

A

Blood = paraprotein IgG or IgA
Urine = Bence Jones Protein

61
Q

How is myeloma define clinically?

A

clonal bone marrow plasma cells account for over 10% of the bone marrow AND end organ damage (CRAB)

1 or more of
Calcium over 2.75
Renal: creatinine clearance less than 40ml/min / creatinine over 177
Anaemia: Hb less than 100g/l
Bone lesions - lytic lesions

62
Q

What is smouldering myeloma

A

thing before multiple myeloma where you have high plasma and/or bence jones or paraprotein cells over 30 but don’t have any organ damage yet

63
Q

What is MGUS?

A

before multiple myeloma where you’re producing the paraprotein but that’s it, paraprotein still under 30 tho

64
Q

Treatment of myeloma

A

MGUS = annual blood test
Smouldering / myeloma = treat

  • Urine bence jones
  • whole body imaging to rule out lytic lesions
  • Stem cell transplant
  • targeted drugs
65
Q

What is Waldenstrom’s macrogloublinaemia

A

like myeloma but IgM is raised and not IgG or IgA

HAEMOTOLOGY (3 decks)

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