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hema finals (week 15) > acute leukemia > Flashcards

acute leukemia Flashcards

1
Q

FAB

CD 13, 33, 14, 4, 11b, 11c, 64, 36, 68

A

FAB M4

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2
Q
  • Is primarily a disease of childhood and adolescence, accounting for 25% of childhood cancers and up to 75%ofchildhood leukemia (most common type of leukemia inchildren)
  • Peak incidence in children is between 2 and 5 years of age; although rare in adults, risk increases with age; most adult patients are older than 50 years of age
  • The subtype is an important prognostic indicator for survival; adults have a poorer outlook: 80% to 90% experience complete remission, but the cure rate is less than 40%
  • Lymphoblasts stain PAS and TdT (+) ;
  • Sudan Black B (SBB) and Myeloperoxidase (MPO) (-)
A

acute lymphoblastic anemia (ALL)

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3
Q
  • SB (+)
  • MP (+)
  • PAS (-)
  • NASDCA (-)
  • a-NA (-)
  • acid phos (-)
A

M1

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4
Q
  • Characterized by the presence of at least >20% (WHO) or >30% (FAB) blasts, of which at least 50% must be of megakaryocyte origin ; Rarest type of AML
  • Cells are stained with Alpha Naphthyl acetate esterase (ANAE) and PAS
  • Markers present: von Willebrand factor, CD41 (gp IIb) , CD42b (gp Ib), CD61 (gp IIIa)
A

FAB M7 (acute megakaryoblastic leukemia)

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5
Q

FAB type

  • patients with leukemia secondary to Burkitt’s lymphoma; t(8;14) → myc oncogene
  • blast: large
  • nuclear shape: regular oval to round
  • nucleoli: prominent, basophilic
  • cytoplasm: prominent, vacuoles
A

L3

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6
Q
  • Similar to t(8;21) (q22;q22.1); RUNX1/RUNX1T1 mutation in WHO classification
  • A common variant that presents with <90%, myeloblasts and >10% maturing cells of neutrophil lineage, and <20% precursors with monocytic lineage
  • Auer rods are often present
  • Most blasts stain with MPO,SBB, and CAE
  • Markers present: CD13, CD33, CD117, CD34
  • FAB M1 and M2 account for 50% of AML cases
A

FAB M2 (w/ maturation)

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7
Q
  • Although morphology is the first tool used to distinguish ALL from AML, (?) and genetic analysis are the most reliable indicators of a cell’s origin
  • Because both B and T cells are derived from lymphoid progenitors, both usually express CD34, terminal deoxynucleotidyl transferase (TdT), and human leukocyte antigen, DR subregion (HLA-DR)
A

immunophenotyping

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8
Q
  • One of the major changes in the 2017 WHO classification is the removal of acute erythroleukemia (erythroid/myeloid type)– most of these cases will now be classified as MDS with excess blasts

ACUTE ERYTHROLEUKEMIA
* Aka known as Erythemic myelosis, Di Guglielmo’s syndrome

  • Characterized by >20% (WHO) or >30% (FAB) marrow myeloblasts and >50% dysplastic marrow normoblasts/erythroblasts

Markerspresent:
* Erythroblasts: CD45, Glycophorin A (CD71)

  • Myeloblasts: CD13, CD15, CD33, CD117
  • Myeloblasts stain positive with SBB, MPO, CAE ; erythroid cells are PAS-POSITIVE

PURE ERYTHROID LEUKEMIA
* characterized by >80% erythroid cells ; >30% proerythroblasts

  • RBC precursors have significant dysplastic features ; presence of ringed sideroblasts, Howell-Jolly bodies and other inclusions
A

FAB M6 (acute erythroleukemia)

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9
Q
  • SB (++)
  • MP (++)
  • PAS (-)
  • NASDCA (+)
  • a-NA (-)
  • acid phos (-)
A

M2

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10
Q

FAB

CD 13, 33, 117

A
  • FAB M0
  • FAB M1
  • FAB M2
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11
Q

immunophenotype

  • t(4;11) , CD10 (CALLA → common ALL antigen)
  • CD34, CD19, CD10, vytoplasmic CD22, TdT
A

intermediate (common) B-ALL

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12
Q
  • affects all ages, but increases with older age (>60 yrs)
  • may resemble acute infection at presentation
  • requires 20% blasts in blood or marrow for diagnosis
  • key myeloid antigens : MPO, CD13, CD33, CD117, ans CD14/CD64
  • recurrent cytogenetic abnormalities that characterize defined subtypes
  • classification made by morphology, cytogenetics, flow cytometry, cytochemistry
A

acute myeloid leukemia

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13
Q

AML

CLINICALFINDINGS:
* Infiltration of (?) into the gums and other mucosal sites and skin

  • (?) is seen in half of AML patients, but (?) is rare
  • (?) is also common at presentation
  • During induction chemotherapy, especially when the WBC count is quite elevated, (?) may occur
A
  • malignant cells
  • splenomegaly, lymph node enlargement
  • hypokalemia
  • lumor lysis syndrome
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14
Q

WHO ALL

have abnormal gene rearrangements, none of the abnormalities is clearly associated with specific biologic features

A

T-lymphoblastic leukemia/lymphoma (T-ALL)

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15
Q

ALL

  • Predominance of (?) (>20% for (?); >30% for (?)) in about 50% of patients (lymphoblasts with lymphocytes and smudge cells)
  • Granulocytopenia

IMMUNOPHENOTYPING:
* B-CELL ALL: CD(?), CD (?),CD (?), CD(?), TdT
* T-CELL ALL: CD(?), CD(?), CD(?), CD(?), CD(?), CD(?), TdT

A
  • blast cells
  • WHO, FAB
  • 34, 19, 10, 22
  • 2, 3, 4, 5, 7, 8
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16
Q
  • May comprise >90% myeloblasts, and fewer than 10% of the leukocytes show maturation to the promyelocyte stage or beyond
  • Atleast 3% of blasts give positive results with myeloperoxidase (MPO) or Sudan black B (SBB) stains ; also stain with CAE
  • Markerspresent: CD13, CD33, CD117, CD34
  • Presence of chloroma → green appearance of tissue using MPO
  • Auer rods maybe present
A

FAB M1 (w/o maturation)

17
Q
  • SB (-)
  • MP (-)
  • PAS (+)
  • NASDCA (+)
  • a-NA (+++)
  • acid phos (-)
A

M6

18
Q

immunophenotype

  • t(9;22) →Philadelphia chromosome
  • MostmatureBcell ALL; TdTnegative, CD34 variable
  • 15%ofchildhoodand 10%ofadult B cell ALL
  • CD34, CD19, cytoplasmic CD22, cytoplasmic u, TdT (variable)
A

pre-B-ALL

19
Q
  • SB (-)
  • MP (+)
  • PAS (+)
  • NASDCA (+)
  • a-NA (+++)
  • acid phos (-)
A

M7

20
Q
  • t(7;11)
  • mostoften in teenaged males with a mediastinal mass, elevated peripheral blast counts, meningeal involvement, and infiltration of extra marrow sites
  • CD2, CD3, CD4, CD5, CD7, CD8, TdT
A

T-ALL

21
Q

FAB

CD 13, 33, 117, 14, 4, 11b, 11c, 64, 68, 36

A

FAB M5

22
Q

FAB type

  • children
  • blast: small
  • nuclear shape: indistinct
  • nucleoli: scant
  • cytoplasm: invisible
A

L1

23
Q

FAB

CD 41, 61, 36, 13, 33

A

FAB M7

24
Q

immunophenotype

  • 5%inchildren and 11%in adults
  • CD34, CD19, cytoplasmic CD22, TdT
A

early (pro/pre-pre) B-ALL

25
Q
  • Account for less than 5% of AML, and patients are generally either infants or older adults
  • Auer rods typically are absent, and there is no clear evidence of cellular maturation
  • Markers present: CD13, CD33, CD34, CD117
  • Cells yield NEGATIVE RESULTS with the cytochemical stains myeloperoxidase (MPO) and Sudan black B (SBB)
A

FAB M0 (minimally differentiated)

26
Q

FAB type

  • older children and adults
  • blast: large, heterogenous
  • nuclear shape: indented, prominent
  • nucleoli: large, abundant
  • cytoplasm: moderately clefted
A

L2

27
Q
  • the most common type of leukemia in adults, and the incidence increases with age
  • is less common in children
A

acute myeloid leukemia (AML)

28
Q
  • Characterized by >20% (WHO) or >30% (FAB) marrow monoblasts ; account for 10% of AML cases
  • In these leukemias, which are divided into monoblastic and monocytic based on the degree of maturity of the monocytic cells present
  • Schilling’s type/AML poorly differentiated/Acute monoblastic leukemia/AML without maturation
  • Seen in children ; >80% monoblasts in the bone marrow
  • Seen in middle-aged adults ; <80% monoblasts
  • Cytogenetic abnormality: t(8;16)(p11;p13) has been associated with M5 (also M4)
  • Markers present: CD14, CD4, CD11b, CD11c, CD 64
  • Cells stain positive with NSE
A

FAB M5 (acute monocytic leukemia)

29
Q
  • Characterized by a significantly elevated WBC count and the PRESENCE OF MYELOID AND MONOCYTOID CELLS in the peripheral blood and bone marrow
  • Characterized by >20% (WHO) or >30% (FAB) marrow myeloblasts with >20%-80% cells of monocytic origin (monoblast, promonocyte, monocyte); may have Auer rods
  • Also called as NAEGELI’S TYPE ; accounts for 30% of AML cases

Markerspresent:
* Myeloid: CD13, CD33, CD34, CD117

  • Monocytic: CD14, CD4, CD11b, CD11c, CD64, CD36, CD68, and lysozyme
  • Myeloid cells stain with SBB, MPO, and CAE , monocytic cells with NSE (non-specific esterase)
A

FAB M4 (acute myelomonocytic leukemia)

30
Q
  • SB (+/-)
  • MP (+/-)
  • PAS (++)
  • NASDCA (-)
  • a-NA (++)
  • acid phos (-)
A

M5

31
Q
  • GOLD STANDARD in classifying leukemias
  • Based on: bone marrow morphology, cytochemical reactions, immunophenotyping, clinical manifestations, cytogenetics (detection of the abnormal gene)
  • CRITERIA FOR DIAGNOSIS OF ACUTE LEUKEMIA: >20% of blasts in the blood is associated with leukemia
A

WHO classification

32
Q
  • SB (+/-)
  • MP (+/-)
  • PAS (-)
  • NASDCA (+/-)
  • a-NA (++)
  • acid phos (-)
A

M4

33
Q

WHO ALL

is subdivided into nine subtypes that are associated with recurrent cytogenetic abnormalities

A

B-lymphoblastic leukemia/lymphoma (B-ALL)

34
Q
  • Refers to the rapid, clonal proliferation in the bone marrow of lymphoid or myeloid progenitor cells knownas lymphoblasts and myeloblasts
  • When proliferation of blasts overwhelms the bone marrow, blasts are seen in the peripheral blood and the patient’s symptoms reflect suppression of normal hematopoiesis
  • Onset is sudden, progression is rapid, and the outcome is fatal in weeks or months if left untreated
A

acute leukemia

35
Q

differentiated based on morphology, including cell size, prominence of nucleoli, and the amount and appearance of cytoplasm

A

FAB classification

36
Q

FAB

glycophorin A in erythroids; CD 13, 33, 117 in myeloblasts

A

FAB M6

37
Q
  • Devised in the 1970’s
  • Based on: Bone marrow morphology, cytochemical reactions, cytogenetics, immunophenotyping
  • CRITERIA FOR DIAGNOSIS OF ACUTE LEUKEMIA: >30% of blasts in the blood is associated with leukemia
A

FAB classification

38
Q
  • Comprises 5% to 10% of AML cases ; occurs in all age groups but is seen most commonly in young adults
  • Characterized by a differentiation block at the promyelocytic stage
  • Thepresence of >30% abnormal promyelocytes with bundles of auer rods (faggot cells)
  • Abnormal promyelocytes can be:
  • Hypergranular → associated with DIC and absence of HLA
  • Hypogranular/Microgranular → aPML-M3v ; 20-30% of APL cases; presence of “butterfly” or coin-on-coin nucleus
  • Promyelocytes stain positive with SBB, MPO, and CAE
  • Cytogenetic abnormality involves balanced translocation between chromosomes 15 and 17 t(15;17) ; fusion of PML gene and retinotic acid receptor alpha (RARa) or the PML-RARa gene
  • 95% of APL cases have the PML-RARa protein
  • Treated with all-trans-retinoic acid (ATRA) and arsenic trioxide
A

FAB M3 (acute promyelocytic leukemia)

hema finals (week 15) (2 decks)

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