L11 Acute Leukemia Flashcards
Comment on the differences in site and spread between leukemia and lymphoma.
- Site
Leukemia: arises from bone marrow
Lymphoma: arises in lymph nodes and extranodal tissues - Spread
- Both can spread to elsewhere like blood
- leukemia: can spread to LN
- lymphoma: can spread to BM
> 20% of blast cells in PB/BM, characterized by continuous proliferation but failure of differentiation
?
Acute leukemia
Typical age of presentation
A. ALL: children and young adults
B: CLL: 40-60 years old
C. AML, CLL: 60+ years old
All except A:
should be old adults
What are the genetic predisposition risk factors for leukemia?
- Down’s syndrome
- Fanconi’s anemia
- Bloom syndrome
Other than genetic predeposition, what are the other risk factors for leukemia?
- Previous exposure to chemotherapy, radiation and chemicals (benzene)
- PMH of MDS or MPN
Suggest the bloom film presentation in acute leukemia patients. (3 typeds of blood cells) > symptoms?
Pancytopenia due to bone marrow failure
- anemia: pallor, fatigue
- thrombocytopenia: bleeding tendency, intracranial hemorrhage, DIC
- neutropenia: infection, fever
***Leukocytosis: hyperviscosity due to increased circulating blasts (to stop other white cells from proliferating, like neutrophil) : visual disturbance, headache, vertigo
Blood viscosity _________ in acute leukemia, why?
increases (hyperviscosity syndrome)
- due to increase in WBC (hyperleukocytosis)
In acute leukemia, there might be possible organ infiltraion.
List 4 examples for ALL.
- Bone pain
- Lymphadenopathy
- Testicular swelling
- CNS symptoms (meningeal involvement)
What is the possible organ infiltration in T-ALL (T cell Acute lymphoblastic leukemia)?
SVCO (SVC obstruction) - mediastinal mass
Which kind of acute leukemia will show clinical symptom of organ filtration in the gum (Gum hypertrophy)?
AML M5
acute monocytic/ monoblastic leukemia
What are the types of acute leukemia under the myeloid lineage?
(6)
- AML related to recurrent genetic abnormalities
- Myeloid proliferations related to Down’s syndrome
- AML with mylodysplastic-related changes
- Therapy-related myeloid neoplasm
- Myeloid sarcoma (extramedullary tumor with myeloblasts)
- AML, NOS (not otherwise specified)
What are the types of acute leukemia under the lymphoid lineage? (3)
- Precursor B cell
- Precursor T cell
- ALL of ambiguous lineage (acute undifferentiated leukemia)
In B-ALL with hyperdiploidy (>50chromosomes) has _____ pronosis.
better
Hypodiploidy: poor prognosis
What are the characteristic features of AML-M3 Acute promyelocytic leukemia (APL)?
- with Auer rods
- DIC
What are the characteristic features of AML-M5 Acute monocytic leukemia?
- without Auer rods
- with gum hypertrophy
Difference in size of morphology of blast in AML and ALL?
AML: big and numerous
ALL: small and few
Which of the following about myeloblast are true?
A. they are big and numerous compared to lymphoblasts
B. they have fine granules
C. they have fine chromatin
D. they have prominent nucleoli
E. absent auer rods
F. Faggot cells are present in APL (promyelocytic leukemia)
All except E
Auer rods +
APL: Faggot cells (= promyelocytes with Auer rods ++)
Which of the following about lymphoblasts are true? A. they have very high N:C ratio B. they have fine chromatin C. they have agranular cytoplasm D. absent auer rods E. indistinct nucleoli
All except B
clumped chromatin
Give 4 examples of myeloid markers.
- CD33
- CD13
- CD17
- MPO (myeloperoxidase)
Give 5 examples of B-lymphoid markers (present in 80% of B-ALL)
- CD10
- CD19
- CD20
- CD22
- CD79a
Give 4 examples of T-lymphoid markers (present in 15% of T-ALL)
- CD2
- cCD3 (cytoplasmic CD3)
- CD5
- CD7
(pneumonic: prime numbers, prime= killing=T cells)
What method is used for diagnosing, finding pathophysiology, treatment and prognosis, even for detecting MRD? (minimal residual disease)
Genetics studies
e.g. G-banding, FISH, molecular genetic study: RT-PCR, NGS
What does PML-RARA indicate in G-banding?
APL
acute promyelocytic leukemia
(FISH can detect it also)
Translocation of chromosomes 9 and 22 + Ph+ =?
B-ALL with poor pronosis
List 3 possible mutations which can be detected by PCR in AML patients. (also list the prognosis)
- FLT3-ITD mutation: poorer prognosis, FLT3 inhibitors under trial
- NPM1 mutation: better prognosis
- CEBPA biallelic/ double mutation: better prognosis
List the possible complications to be screened in acute leukemia patients.
- DIC in APL
- Extra-medullary involvement (myeloid sarcoma: biopsy/ lumbar puncture: ALL)
- Tumor-lysis syndrome (TLS)
- Septicemia: blood culture
General treatment for APL/ALL patients?
- Chemotheraphy
- APL: ATRA (all-trans retinoic acid), arsenic trioxide - Gene-targeted therapy
- tyrosine kinase injibitor for BCR-ABL-1 + ALL - Chemotherapy + Allogenic stem cell transplantation
- poor prognosis cases
How is acute promyelocytic leukemia treated? (APL)
=AML-M3
- before definite genetic diagnosis is reached (PML-RAR):
- ATRA (tretinoin) based on clinical and morphological (faggot cells) crieteria - PML-RARA:
- ATRA to promote differentiation
- Arsenic trioxide to promote apoptosis
How is APL monitored?
RQPCR of PML-RARA (minimal residue disease MRD)
Difference between acute and chronic leukemia?
Acute leukemia: accumulation and proliferation of precursor cells or undifferentiated cells
Chronic leukemia: accumulation and proliferation of mature and differentiated cells
Plasma cell myeloma is resulted from clonal proliferation of?
Plasma cells
What are the other possible diseases that mimic acute leukemia clinically?
- Aplastic anemia
2. Marrow infiltration by other malignancies
