Leukemias Flashcards
Types of AML (3)
- Myeloblastic
- Monoblastic
- Megakaryoblastic
Difference between acute and chronic leukemias
Acute: very immature, very fast
Chronic: more similar to mature, slow
Diagnosis of AML
Blast cells >20% or genetic anomalies
Causes of AML (3)
- Increase proliferation
- Decrease apoptosis
- Block differentiation
AML age group
> 65 years
10-15% childhood
AML immunophenotype (4)
CD13+ CD33+ CD117+ TdT-
AML clinical features (4)
- Infections: Candida, Pseudomonas
- Normo normo anemia
- Thrombocytopenia + DIC = bleeding = BRUISES (PML)
- Gum hypertrophy
What are Auer rods made of and in which leukemia are they found?
MPO
Myeloid leukemias
AML mutations (3)
t(8:21) —> RUNX1/CBF1b —> block maturation
t(15:17) —> RARa-PML —> interfere with terminal differentiation = PML
FLT3 —> signals that there’s normal growth —> PML
AML mutation with the best prognosis
t(15:17) / PML
What differentiates PML from AML?
***Coagulopaties
Phenotype is arrested differentiation
Best prognosis
Labs in PML
Options: cancer procoagulant, factor V, FDP, fibrinogen, D-dimers, platelets, thrombin
Decreased:
- Fibrinogen
- Factor V
- Platelets
Increased:
- FDP
- D-dimers
- CP
- Thrombin generation
What is the mechanism of coagulopathies in PML? What is the activator called?
HYPERFIBRINOLYSIS
- Increase in degradation products
- Decrease in inhibitors: PAI-1, a2 antiplasmin
Annexin A2 = fibrinolytic activator ANA1
Myelodysplastic syndrome why are they considered “pre-leukemia”?
They only stop maturation, don’t get posterior mutations
Why do myelodysplastic syndromes rarely turn into AML?
Patients die
How to differentiate between AML and MDS?
Blast amount
Normal: 2-3%
MDS: <20%
AML: >20%
ALL age group
CHILDHOOD (3-7)
Which leukemias are Tdt +?
ALL
CLL
Most common ALL mutations (6)
t(9;22) - adult
t(12;21) - kids
MLL rearrangements
Diploidy
Abnormal karyotype
NOTCH signaling
ALL clinical features (blood 3 and organs 6)
- Anemia normo normo
- Neutropenia = infections, fever
- Thrombocytopenia = bruises, purpura
- Tender bones
- Lymphadenopathy
- Hepatosplenomegaly
- Papilloedema
- Meningeal sx
- Rare testicular swelling
ALL labs
Decrease: cells
Increase:
- Uric acid
- LDH
- Ca2+
t(9;22) mutation:
- Leukemia type
- Age group
- Gene
- Prognosis
“Philadelphia gene”
1. ALL
2. Adults
3. BCR-ABL1
4. Poor prognosis