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Acute Leukaemia - Coggle Diagram
Acute Leukaemia
DX
Hx&exam
S&s of cytopenias+organ infiltration
FBC
cytopenias+/-^WCC
blood smear
large blasts
high nuclear:cytoplasmic ratios
fine chromatin
AML
auer rods
azurophilic granules
bundles seen in APML
if DIC too=emergency
morphology
AML
M0-M7
ALL
L1-3
biochemistry
^LDH
^uric acid
coagulation
APML/rare subtypes
DIC
Blood group+/-cross matching
CXR
Septic screen if febrile
bm aspirate/biopsy
smear
flow cytometry
antigen expression
AML
MPO
CD117
CD33
CD13
CD14/64
B-ALL
CD19
CD79a
CD10
CD22
T-ALL
CD3
CD7
CD5
CD1a
cytogenetics
G-banding
numerical abnormalities
hyperdiploidy
good prognosis in ALL
monosomy 7
poor prognosis in AML
FISH
translocations
t(9:22) - BCRABL
B-ALL
CML
targeted by imatinib/newer gen.
molecular characterisation
tests for genetic alteration that change management
comprehensive genetic characterisation
whole genome sequencing/trancriptomics
Treatment
first day
bm aspirate
lumbar puncture+intrathecal chemo
insertion of central venous catheter
ALL
4 high dose chemo over 9mths
maintenance
3 monthly intathecal treatment
2yrs
low dose chemo
2-3 yrs
improvement
short term
risk stratification
tailored treatment
medium to long term
better understanding of mechanism
targeted treatments
MRD
targets identified
Ig/TCR gene rearrangement
AO-QPCR
leukaemia associated phenotype
determined by flow cytometry
response dictates further treatment
leukaemia still detected
need more intensive therapy
targeted
BCR-ABL
imatinib/dasatinib/nilotinib/ponatinib
APML
AsO3 and retinoic acid
chemo free
immunotherapies increasingly important
CAR-T
chimeric antigen receptor
cells engineered to express receptor
targets cancer cells for destruction
hard to treat leukaemias
anti-CD19 therapy
tisagenlecleuce/Kymriah
General
immature cells
ALL incidence peaks in childhood
AML incidence increases with age
harbours recurrent genetic alterations
usually in genes regulating haematopoiesis
mutations impair normal function
block in blood cell differentiation
genetics vary greatly with age
Presentation
compromised haematopoiesis
reduced Hb
fatigue
decreased energy
dyspnoea
reduced WCC
infections
reduced platelets
easy bruising
bleeding
organ infiltration
mediastinal mass
T-ALL/T-NHL
hepatosplenomegaly
lymphadenopathy
rare
gum infiltration
monoblastic AML
skin lesions
AML
myeloid sarcoma/chloroma
leukocytosis
testis
Systemic symptoms
generally unwell
tired
temperatures
bone pain