Acute Leukemias Flashcards Preview

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Flashcards in Acute Leukemias Deck (33):
1

CBC chart diagram

WBC, Hgb/Hct, Platelets

2

acute leukemia

abrupt onset of pancytopenia (decrease in all cell types). dysfunctional immature neoplastic cells replace everything. quickly become sick

3

acute

immature neoplastic cells predominate

4

chronic

mature neoplastic cells predominate

5

what types of leukemias are better prognostically?

acute better than chronic
myeloid better than lymphoid

6

myeloproliferative neoplasms (MPNs)

clonal expansion of an abnormal hematopoietic stem cell with retained differentiation leading to expansion of mature hematopoietic cells. can become ALL or AML

7

subtypes of myeloproliferative neoplasms

polythemia vera, essential thrombocytosis, chronic myeloid leukemia, chronic idiopathic myelofibrosis (RBCs, platelets, neutrophils, megakaryocytic respectively)

8

myelodysplastic syndrome

clonal expansion of an abnormal HSC with abnormal differentiation leading to decreased number of mature hematopoietic cells, resulting in anemia, thrombocytopenia, or neutropenia. can lead to AML (rarely ALL)

9

what types of chemotherapy can lead to acute leukemia?

alkylating agents (cyclophosphamide) or topoisomerase 2 inhibitors (etoposide, doxorubicin)

10

acute leukemia transformation

can arise from MDS, MPNs, and clonal marrow failure syndromes

11

most common childhood cancer?

ALL acute lymphocytic leukemia

12

how do leukemias arise?

marrow is constantly turning over cells in order to maintain normal blood cell pools. unfortunately gives more chances for mutations to occur. in acute leukemias, these occur at proliferative stage, blocking maturation somehow

13

who has an increased chance of getting acute leukemia?

children with inherited errors of dna repair

14

clinical definition of MDS

acquired, persistent reduction in circulating myeloid blood cell counts with abnormal blood cell morphology. indolent growth

15

MDS marrow morphology

hypercellular marrow, increased apoptosis. hypo granular granulocytic precursors. hypolobated, micromegakaryocytes. increased marrow blasts.

16

what types of mutations lead to acute leukemias?

nonrandom, multiple ones: recurrent chromosomal abnormalities and gene mutations seen.

17

APL (acute promyelocyte leukemia)

AML with t(15;17). fuses PML TF with retinoid acid receptor RARa, which then strongly binds DNA and recruits histone deacetylases, leading to transcription repression and maturational arrest.

18

treatment for APL

all-trans retinoid acid (ATRA). ligand for PML-RARa that restores transcription and induces cell maturation.

19

prognosis for ALL (childhood vs adult)

childhood ALL cured by intensive chemotherapy. Very difficult to cure in adults.

20

clinical symptoms of leukemia

fatigue, fever, infection, bleeding, lymph node enlargement, bone pain due to marrow expansion, cranial neuropathy (involvement of spinal fluid), testicular masses

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clinical consequence of APL

highly dangerous bleeding risk

22

why is cancer in testes particularly bad?

chemotherapy can't gain access, must be radiated, which sterilizes

23

signs of leukemia

pallor, petechial rashes, splenomegaly, swollen gums

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leukostasis

rare but serious complication of leukemia in which too many WBCs in circulation cause a leukothrombosis

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how can you distinguish AML for ALL

flow cytometry

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cytologic abnormality in AML

Aeur rods in cytoplasm

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Aeur rods

aggregates of myeloperoxidase that form cytoplasmic needle like inclusions.

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B lymphoid lineage immunophenotype

CD19, CD79a, Ig

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T lymphoid lineage immunophenotype

CD2,3,4,7

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myeloid lineage immunophenotype

CD13, 33, myeloperoxidase (MPO)

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best predictor for treatment response and survival for acute leukemias?

karyotype

32

favorable AML karyotypes

t(15;17) (PML treat with ATRA)
t(8;21)
inv16

33

acute leukemia

hematologic malignancy in which rapidly progressive marrow failure occurs