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103 theme 3 > leukaemia > Flashcards

leukaemia Flashcards

1
Q

what is haematopoesis

A

marrow - myeloblast-promuelocyte-myelocyte-metamyelocyte-band neutrophil-neutrophil (blood to tissue) or myeloblast-promonocyte-monocyte(blood)-immaure macrophage-mature macrophage(tissue)

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2
Q

what is G-CSF

A 
granulocyte colony stimulating factor 
promotes neutrophils  (main driving factor)
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3
Q

what growth factors affect white blood cells

A

bone marrow maturation - SCF, G-CSF, IL-3, GM-CSF

Allow tissue migration

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4
Q

what is cancer

A

transformed cell phenotype (uncontrolled proliferation, failure to undergo apoptosis)
genetic (mutations in oncogenes, tumour suppressor genes)
epigenetic (deregulated gene expression, aberrant DNA methylation)

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5
Q

what are types of mutations that occur

A 
point (change AA seq)
translocation
partial chromosome deletion 
chromosomal duplication
dan methylation or deacetylation of histones surpasses gene transcription
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6
Q

what is the clonal evolution of leukaemia

A

take a while to emerge as cancer undergoes clonal selection to turn from normal to malignant clones

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7
Q

what are the clinical features of the 3 myeloproliferative disorders

A

polycythemia rubra vera
myelofibrosis
essential (massive splenomegaly) thrombocythemia
leucoerythroblastic blood film picture

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8
Q

what is the JAK-STAT signalling (pathway for EPO and G-CSF)

A

acquired mutation in JAK-2 gene transmitted to receptor so switched on to result in the 3 conditions
can all progress to acute myeloid leukaemia

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9
Q

what is the mutation in the JAK-2 gene

A 
the same for all 3
JAK2 V617F (g to t)
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10
Q

what are treatments of MPDs

A

reduce spleen size

lower Hb, platelets and WBC counts

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11
Q

what is chronic myeloid leukaemia

A

too many white cells
Buffy coat expanded in blood sample
translocation philadelphia chromosome (9;22)

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12
Q

how is CML diagnosed

A

FISHing for CML
FLUORESCENT IN STIU HYBRIDISATION
Translocation event of 9;22

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13
Q

what other DNA mutations can contribute to CMLF

A

BCR-ABL oncogene

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14
Q

what is the major CML treatment

A

imatinib
targeted therapy to bind to BCR-ABL oncoprotein - normalises white cell count and improves CML survival (over 90% from 50% after 5 years)

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15
Q

what can CML occasionally do

A

transforms to AML

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16
Q

What is acute myeloid leukaemia

A

uncontrolled proliferation of primitive cells in bone marrow
causes failure - anaemia, infections, bleeding
blasts identified on blood film (mitosis, large nucleus)

17
Q

what are the clinical features of AML

A 
anaemia 
infections
DIC
Ulcers
Infiltration 
bruising
18
Q

how is AML diagnosed

A 
bone marrow biopsy 
morphology
immunophenotyping
genetic
cytogenetic
molecular
19
Q

how is AML treated

A

chemotherapy - kills rapidly dividing cells, combo regimes, myeloid-ablative cycles of treatment

20
Q

how can AML be treatment by allogenic stem cell transplantation

A

allograft (full or reduced intensity)
slibling (1 in 4 chance of match)
matched unrelated donor

21
Q

what are supportive measures for AML treatment

A

transfusions (RBCs, Ps, Cryo/FFP)
AB (prophylactic, broad spec)
Antifungals

22
Q

what is the aim of chemo

A

drive cell count low enough for body’s immune system to deal with it
transfusions to deal with each cycle
age and genetics also play a role

23
Q

what is allogeneic transplantation

A

new bone marrow (harvest stem cell from matched donor) infused into patient (conditioned by chemo so donor cells can take up residence)
also needs intensive support, immunosuppression and close monitoring

24
Q

what can result from allogeneic transplantation

A

opportunistic infections
Fungal infections
pneumocystis pneumonia

25
Q

what is neutropenic sepsis

A 
ME
Gram -ve bacteria most dangerous 
blood cultures and blind antibiotic therapy if fever (Tazocin, meropenem, add AF)
iv fluids if hypotensive
inotropic support on ITU
26
Q

what is graft vs host disease

A

donor/host mismatches in major and minor HLA loci
rejection reactions - skin rash, diarrhoea, deranged liver function
acute GVH and chronic GVH post transplant

27
Q

what is graft vs leukaemia

A

how stem cell transplant cures leukaemia

28
Q

how can graft vs host disease be treated

A

T-cell depletion of infused donor cells (graft)
Immunosuppression of recipient (ciclosporin)
Donor lymphocyte infusions (DLI) post-Tx can treat relapse by augmenting GVL effect

29
Q

what gene can also cause AML

A

DNMT3A methyltransferase

103 theme 3 (20 decks)

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