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Z MD1 Intersystems > leukaemia and lyphoma > Flashcards

leukaemia and lyphoma Flashcards

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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
what are the types of chronic leukaemia
chronic lymphocytic leukaemia chronic myeloid leukaemia hairy cell leukaemia chronic myelomonocytic leukaemia
26
common symptoms of leukaemia
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
27
which CD markers are typical for CLL
CD19 and CD5
28
what do you see on a histological slide in someone who has CML
leukocytosis with a left shift
29
what is typical for ALL on histological slide
blasts - with no Auer rods or granules
30
what is the common translocation that causes AML
t(15:17)
31
how does imatinib work
- inhibits BCR-ABL autophosphorylation and phosphorylation - induces apoptosis - inhibits proliferation
32
what is ABT-199
selective Bcl-2 inhibitor for treatment of CLL
33
what enters/exits the lymph node at the hilum
enters = artery exits = vein and lymphatics
34
where does the lymphatic vessels enter the lymph node
around the outside of the node through the capsule through afferent lymphatic
35
what is the histological "sign" of an active lymph node
germinal centres in the cortex
36
what things are found in the paracortex of the lymph node
naive T cells high endothelial venules interdigitating dendritic cells
37
what is a primary follicle of the lymph node
follicle of B cells that are unactivated
38
what things are found in primary follicles
naive B cells follicular dendritic cells t cells
39
what things are found in the mantle zone
Naive B cells
40
where is the mantle zone
directly around the germinal centres
41
how do the T cells come into the lymph node
via endothelial venules
42
what are the "markers" for immunohistochemistry for B and T cells
B = CD20 T = CD3
43
what is the differentiation steps between a naive B cell and a plasma cell
centroblasts --\> centrocytes --\> immunoblasts --\> plasma cells
44
where does maturation of the B cells occur
naive B cell --\> immunoblasts in germinal centre final maturation into plasma cells in medullary cords
45
what are the 2 major causes of lymphadenopathy
reactive inflammatory and infective neoplastic
46
when do you see acute non-specific lymphadenitis
nodes draining directly from a microbial infection
47
what are the histological signs of acute non-specific lymphadenitis
neutrophil infiltration, oedema, follicular hyperplasia
48
what is the difference in the presentation between acute and chronic non-specific lymphadenitis
acute = nodes large and painful chronic = generally non tender
49
what are the 5 broad causes of non-specific lymphadenitis
follicular hyperplasia (humoral response) paracortical (cellular response) sinus histiocytosis (non-specific) granulomatous inflammation mixed
50
what are the causes of neoplastic lymphadenopathy
primary tumour: Hodgkins or non-Hodgkins secondary tumours (metastases) leukaemic infiltration
51
what are the histological signs of Hodgin lymphoma
Reed Sternberg cells neoplastic germinal centre B cells
52
risk factors for lymphoma
- immunosuppresion or ID - some autoimmune diseases - EBC, H pylori - environmental
53
what causes Burkitt's lymphoma
translocation (3:8) --\> overproduction of MYC oncogene
54
what are the B symptoms of lymphoma
temperature \>38 night sweats weight loss \>10% from baseline in 6 months
55
what do Reed-Sternberg cells look like
large cell with abundnant cytoplasm and a large bilobate nucleus with prominent eosinophilic nucleoli
56
is B or T cell non-hodgkins lymphoma more common
B
57
58
which leukaemia is associated with philadelphia chromsome
CML
59
What is the important GF for the early progenitor haematopoietic cells
c-Kit
60
how is the cell cycle told to start
activation via cytokine Receptor --\> activates intracellular signalling --\> transcription factor activation --\> activates Cyclin D --\> activates CDK4 --\> activates G1
61
what are the 6 hallmarks of cancer
- autonomous growth signalling - evading growth inhibitory signals - evasion of apoptosis - activating invasion and metastasis - angiogenesis - immortality
62
which leukaemias/lymphomas are due to autonomous growth signalling
CML ALL Burkitt's lymphoma
63
Which leukaemias/lymphomas are due to an evasion of apoptosis
CLL
64
Which leukaemia/lymphoma is due to evasion of growth inhibitory signals
burkitt's lymphoma
65
what are the 4 emerging hallmarks of cancer
- deregulating cellular energetics - avoiding immune destruction - tumour promoting inflammation - genome instability and mutation
66
what makes lymphoid cells sensitive to mutations
- 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
What is the difference between myelodysplastic syndromes and myeloproliferative disorders
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
mean survival of CML without treatment
3 years
69
what kind of cells do you get during a blast crisis of CML
myeloid origin or pre-B origin
70
What is the translocation of the philadelphia chromosome
9:22 (Bcr-Abl) Abl = chromosome 9 Bcr = chromosome 22
71
affect of Bcr-abl translocation
causes mostly increased proliferatin and survival of haematopoietic cells
72
action of gleevac
specific inhibitor of BCR-ABL
73
why is it not possible to cure someone of CML from Gleevec
the progenitor cells that give rise to the proliferating CFUs do not cycle often and therefore the treatment cannot target them
74
75
what causes the blast crisis in CML
further mutations in the cells with philadelphia chromosome leading to:
76
which cells area affected in CLL
naive B cell or memory B cell in germinal centre
77
what is the cause of CLL
loss of regulatory miRNA 15a and 16-1 that lead to high levels of Bcl-2, leading to failure of cells to apoptose
78
Which specific further mutations can lead to a worser outcome for a patient with CLL
ZAP-70 and p53
79
what is the lymphoma that is pretty much the same as CLL
SLL (small lymphocytic lymphoma)
80
what do you see in the lymph node with CLL
- loss of normal lymph node architecture due to infiltration of small round lymphocytes
81
which mutations (initial and subsequent) act at which different places of the cell cycle for CLL
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
explain the new up and coming treatment for CLL
ABT-199 = BH3 only drug that inhibitors Bcl-2
83
how does elevated Bcl-2 cause reduced apoptosis
causes a closed channel in the mitochondrial membrane preventing the escape of cytochrome c (therefore cannot activate executioner caspases needed for apoptosis)
84
functions of p53
- 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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