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Z MD1 Intersystems > leukaemia and lyphoma > Flashcards

leukaemia and lyphoma Flashcards

1
Q

which cells are myeloid lineage and which are lymphoid lineage

A

lymphoid - B, T and NK cells

myeloid - the rest

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2
Q

difference between leukemia and lymphoma

A

leukaemia - spills into peripheral blood from bone marrow

lymphoma - more discreet in tissues, hardly any involvement of blood

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3
Q

what are the 5 types of lymphocytic malignancies

A

acute lymphocytic leukemia

chronic lymphocytic leukemia

hodgkin’s lymphoma

non-hodgkin’s lymphoma

plasma cell dyscrasias

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4
Q

what are the 3 types of myeloid malignancies

A

acute myeloid leukemia

myelodysplasic syndromes

myeloproliferative conditions

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5
Q

classic presentation of acute leukemia

A

bone pain

pancytopenia (fatigue, infection, fever, bleeding, bruising)

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6
Q

which blood cell malignancy is the most common in children

A

ALL

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7
Q

cure rate of ALL

A

80% in children

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8
Q

which blood cell malignancy is the most common leukemia in the western world in adults

A

CLL

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9
Q

what is the most common presentation of CLL

A

lymphadenopathy

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10
Q

how can CLL be cured

A

allogenic transplant

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11
Q

what is typical for CLL on a histological slide

A

Smudge cells

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12
Q

what is the difference between Hodgkins and non-Hodgkins lymphoma in respect to where it is

A

Hodgkins = typically localised to a single axial group

non-H = usually involves multiple nodes, including peripheral nodes

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13
Q

what what is the difference between Hodgkins and non-Hodgkins lymphoma in respect to spread

A

Hodgkins = orderly pattern of contiguous spread from one group of nodes to the next

Non-H = non-contiguous pattern of spread

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14
Q

what is the difference between Hodgkins and non-Hodgkins lymphoma in respect to mesenteric nodes and Waldeyers ring

A

Hodgkins = rarely involves it

Non-Hodgkins = often involved

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15
Q

what is typical for hodgkins lymphoma on histological slide

A

Reed-Sternberg cells (large cells, multinucleated with multiple nuclear lobes)

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16
Q

what is typical for AML on histological slide

A

blasts with Auer rods

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17
Q

what causes CML

A

philadelphia chromosome t(9;22)

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18
Q

treatment of CML

A

imatinib = inhibitor of the tyrosine kinase receptor

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19
Q

3 structural components of a Lymph node

A

stroma

lymphatic sinuses

vascular

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20
Q

where are the B and T cells located in a lymph node

A

cortex = B cells

paracortex = T cells

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21
Q

what is in the medulla of a lymph node

A

network of lymphatic sinuses, drain into efferent lymphatics

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22
Q

what is the pathogenesis of leukaemia

A

somatic mutatinos in a multipotential primitive cell/more differentiated progenitor cell resulting in a gene which encodes for a protein that disrupts normal cell pathway (and therefore predisposes to malignant transformation)

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23
Q

what is the difference between acute and chronic leukaemia

A

acute = proliferation/accumulation of blasts

chronic = accumulation of maturer white cells

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24
Q

which out of Acute or chronic leukaemia is more serious

A

acute - rapid clinical course and fatal if untreated

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25
Q

what are the types of chronic leukaemia

A

chronic lymphocytic leukaemia

chronic myeloid leukaemia

hairy cell leukaemia

chronic myelomonocytic leukaemia

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26
Q

common symptoms of leukaemia

A

weight loss, fever, frequent infections

easy SOB

weakness

bone pain or tenderness

fatigue, loss of appetidie

lymphadenopathy

hepatosplenomegaly, splenomegaly

night sweats, easy bleeding/brusing, purplish spots

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27
Q

which CD markers are typical for CLL

A

CD19 and CD5

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28
Q

what do you see on a histological slide in someone who has CML

A

leukocytosis

with a left shift

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29
Q

what is typical for ALL on histological slide

A

blasts - with no Auer rods or granules

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30
Q

what is the common translocation that causes AML

A

t(15:17)

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31
Q

how does imatinib work

A
  • inhibits BCR-ABL autophosphorylation and phosphorylation
  • induces apoptosis
  • inhibits proliferation
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32
Q

what is ABT-199

A

selective Bcl-2 inhibitor for treatment of CLL

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33
Q

what enters/exits the lymph node at the hilum

A

enters = artery

exits = vein and lymphatics

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34
Q

where does the lymphatic vessels enter the lymph node

A

around the outside of the node through the capsule through afferent lymphatic

35
Q

what is the histological “sign” of an active lymph node

A

germinal centres in the cortex

36
Q

what things are found in the paracortex of the lymph node

A

naive T cells

high endothelial venules

interdigitating dendritic cells

37
Q

what is a primary follicle of the lymph node

A

follicle of B cells that are unactivated

38
Q

what things are found in primary follicles

A

naive B cells

follicular dendritic cells

t cells

39
Q

what things are found in the mantle zone

A

Naive B cells

40
Q

where is the mantle zone

A

directly around the germinal centres

41
Q

how do the T cells come into the lymph node

A

via endothelial venules

42
Q

what are the “markers” for immunohistochemistry for B and T cells

A

B = CD20

T = CD3

43
Q

what is the differentiation steps between a naive B cell and a plasma cell

A

centroblasts –> centrocytes –> immunoblasts –> plasma cells

44
Q

where does maturation of the B cells occur

A

naive B cell –> immunoblasts in germinal centre

final maturation into plasma cells in medullary cords

45
Q

what are the 2 major causes of lymphadenopathy

A

reactive inflammatory and infective

neoplastic

46
Q

when do you see acute non-specific lymphadenitis

A

nodes draining directly from a microbial infection

47
Q

what are the histological signs of acute non-specific lymphadenitis

A

neutrophil infiltration, oedema, follicular hyperplasia

48
Q

what is the difference in the presentation between acute and chronic non-specific lymphadenitis

A

acute = nodes large and painful

chronic = generally non tender

49
Q

what are the 5 broad causes of non-specific lymphadenitis

A

follicular hyperplasia (humoral response)

paracortical (cellular response)

sinus histiocytosis (non-specific)

granulomatous inflammation

mixed

50
Q

what are the causes of neoplastic lymphadenopathy

A

primary tumour: Hodgkins or non-Hodgkins

secondary tumours (metastases)

leukaemic infiltration

51
Q

what are the histological signs of Hodgin lymphoma

A

Reed Sternberg cells

neoplastic germinal centre B cells

52
Q

risk factors for lymphoma

A
  • immunosuppresion or ID
  • some autoimmune diseases
  • EBC, H pylori
  • environmental
53
Q

what causes Burkitt’s lymphoma

A

translocation (3:8) –> overproduction of MYC oncogene

54
Q

what are the B symptoms of lymphoma

A

temperature >38

night sweats

weight loss >10% from baseline in 6 months

55
Q

what do Reed-Sternberg cells look like

A

large cell with abundnant cytoplasm and a large bilobate nucleus with prominent eosinophilic nucleoli

56
Q

is B or T cell non-hodgkins lymphoma more common

A

B

57
Q
A
58
Q

which leukaemia is associated with philadelphia chromsome

A

CML

59
Q

What is the important GF for the early progenitor haematopoietic cells

A

c-Kit

60
Q

how is the cell cycle told to start

A

activation via cytokine Receptor –> activates intracellular signalling –> transcription factor activation –> activates Cyclin D –> activates CDK4 –> activates G1

61
Q

what are the 6 hallmarks of cancer

A
  • autonomous growth signalling
  • evading growth inhibitory signals
  • evasion of apoptosis
  • activating invasion and metastasis
  • angiogenesis
  • immortality
62
Q

which leukaemias/lymphomas are due to autonomous growth signalling

A

CML

ALL

Burkitt’s lymphoma

63
Q

Which leukaemias/lymphomas are due to an evasion of apoptosis

A

CLL

64
Q

Which leukaemia/lymphoma is due to evasion of growth inhibitory signals

A

burkitt’s lymphoma

65
Q

what are the 4 emerging hallmarks of cancer

A
  • deregulating cellular energetics
  • avoiding immune destruction
  • tumour promoting inflammation
  • genome instability and mutation
66
Q

what makes lymphoid cells sensitive to mutations

A
  • prone to mutations during antibody diversification with the enzyme AID
  • infection with EBC or H pylori leads to long term survival of cells –> secondary chronic inflammation = cancer
67
Q

What is the difference between myelodysplastic syndromes and myeloproliferative disorders

A

MD = cytopenia from disorderly proliferation in BM and a lack of mature cells in blood

MP = increased production in 1 or 2 categories of mature cells

68
Q

mean survival of CML without treatment

A

3 years

69
Q

what kind of cells do you get during a blast crisis of CML

A

myeloid origin or pre-B origin

70
Q

What is the translocation of the philadelphia chromosome

A

9:22

(Bcr-Abl)

Abl = chromosome 9

Bcr = chromosome 22

71
Q

affect of Bcr-abl translocation

A

causes mostly increased proliferatin and survival of haematopoietic cells

72
Q

action of gleevac

A

specific inhibitor of BCR-ABL

73
Q

why is it not possible to cure someone of CML from Gleevec

A

the progenitor cells that give rise to the proliferating CFUs do not cycle often and therefore the treatment cannot target them

74
Q
A
75
Q

what causes the blast crisis in CML

A

further mutations in the cells with philadelphia chromosome leading to:

76
Q

which cells area affected in CLL

A

naive B cell or memory B cell in germinal centre

77
Q

what is the cause of CLL

A

loss of regulatory miRNA 15a and 16-1 that lead to high levels of Bcl-2, leading to failure of cells to apoptose

78
Q

Which specific further mutations can lead to a worser outcome for a patient with CLL

A

ZAP-70 and p53

79
Q

what is the lymphoma that is pretty much the same as CLL

A

SLL (small lymphocytic lymphoma)

80
Q

what do you see in the lymph node with CLL

A
  • loss of normal lymph node architecture due to infiltration of small round lymphocytes
81
Q

which mutations (initial and subsequent) act at which different places of the cell cycle for CLL

A

elevated Bcl-2 = prevents apoptosis induced by p53

elevated ZAP-70 = causes autonomous signalling (no longer need receptor activation)

loss of p53 = prevents DNA repair, apoptosis and inhibition of the cell cycle by p16

82
Q

explain the new up and coming treatment for CLL

A

ABT-199 = BH3 only drug that inhibitors Bcl-2

83
Q

how does elevated Bcl-2 cause reduced apoptosis

A

causes a closed channel in the mitochondrial membrane preventing the escape of cytochrome c (therefore cannot activate executioner caspases needed for apoptosis)

84
Q

functions of p53

A
  • cell cycle arrest (to be able to repair mutations)
  • activates repair processes
  • directs a cell to apoptose if unable to fix mutation

Z MD1 Intersystems (10 decks)

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