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Hematology Block 3 > Leukemia > Flashcards

Leukemia Flashcards

(59 cards)

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1
Q

Leukemias are neoplasms of ____

A

hematopoietic cells

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2
Q

Leukemias have significant ____ and ____ involvement

A

peripheral blood and bone marrow

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3
Q

What is seen in this image?

A

This is a normal bone marrow biopsy

See normal architecture

See mixture of cell types

Appropriate amount of fat cells

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4
Q

What does the presence of a CD34 marker tell you?

A

This means the cell is IMMATURE!

These are present on hematopoietic stem cells

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5
Q

T cells have WHAT CD markers?

A

Low numbers!

CD 1, 2, 3, 4, 5, 7, 8

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6
Q

CD 13:

A

Mid-teens = Myelomonocytic

CD 13 = granulocyte

(GMG = 13, 14, 15)

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7
Q

CD 14:

A

Mid-teens = Myelomonocytic

CD 14 = monocytic

(GMG = 13, 14, 15)

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8
Q

CD 15:

A

Mid-teens = Myelomonocytic

CD 15 = granulocyte

(GMG = 13, 14, 15)

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9
Q

B cells are characterised by what CD markers?

A

CD 19, 20, 21, 22, 23

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10
Q

CD 33:

A

myeloid marker

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11
Q

Co-expression of CD5 and CD20:

A

Indicates CLL - this is not a normal finding!!!

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12
Q

Immunophenotyping:

A

Identifying the phenotype using fluorexcently labeled antibodies (probe)

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13
Q

CML is a ______ disorder (as are P vera, ET, and primary myelofibrosis)

A

myeloproliferative disorder

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14
Q

Describe the cell types generated/found in CML:

A

Hit occurs at hematopoietic stem cell

Cells maintain the ability to differentiate

Morphologically heterogenous population of cells at all levels of myeloid differentiation.

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15
Q

Common symptoms, physical exam findings, and lab findings of CML patients:

A

Common symptoms:

  • Fatigue, sweats, fevers
  • Weight loss/anorexia
  • Abdominal fullness, early satiety

Physical exam findings:

  • Splenomegaly
  • Hepatomegaly

Common laboratory findings:

  • Leukocytosis (neutrophilia, basophilia, eosinophilia)
  • Anemia
  • Thrombocytosis

20-40% of patients are asymptomatic!

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16
Q

Peripheral blood smear and bone marrow findings of CML patients:

A

Peripheral blood:

  • numerous immature granulocytes
  • Increased basophils

Bone marrow:

  • hypercellular
  • Increase M:E
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17
Q

Is this bone marrow biopsy normal?

What disease is suspected?

A

This is abnormal

See a bunch of maturing granulocytes, with almost no fat at all.

CML

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18
Q

t(9;22) is characteristic of WHAT disease processes?

A

t(9;22) is the Philadelphia chromosome, which is present in 95% of CML cases.

Can also be found in ALL, where it has a super bad prognosis

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19
Q

t(9;22) fuses what genes? What is the functional result?

A

Fuses BCR and ABL

ABL is a tyrosine kinase signal transducer - this fusion promotes constitutive cell signaling.

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20
Q

What is the best screening test for CML?

A

FISH

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21
Q

What is a CML blast crisis?

A

This occurs when the disease is left untreated, and cells gain additional genomic hits. This results in the formation of an acute leukemia, characterized by constitutional symptoms, complications of cytopenias, extramedullary disease, etc.

Median survival: 3-6 months

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22
Q

What are the treatment options for CML? What are the outcomes?

A

First line treatment - ABL tyrosine kinase inhibitors (such as Imatinib aka Gleevec). These work super well.

Could also consider allogenic stem cell transplant

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23
Q

CLL (chronic lymphocytic leukemia) is a malignancy of _____

A

mature B cells

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24
Q

In CLL, the malignant cells are a morphologically _______ population of ______

Study These Flashcards
A

In CLL, the malignant cells are a morphologically homogenous population of mature lymphocytes

25
What are common symptoms, physical exam findings, and common lab findings associated with CLL?
Common symptoms: * Fatigue, fevers, sweats * Weight loss/anorexia * abdominal fullness, early satiety * Frequent infection (respiratory; encapsulated) * Asymptomatic in about 20% Physial Exam: * Lymphadenopathy * Splenomegaly * Hepatomegaly Common Lab Findings: * Leukocytosis (**lymphocytosis**) * Anemia * Thrombocytopenia * Hypogammaglobulinemia (even though lots of B cells produced, the cells are mutant and crowd out the Ig-producing B cells, causing hypogammaglobulinemia and infection)
26
What complication is often found in CLL patients?
Autoimmune hemolytic anemia B cells that are able to still produce Ig produce bad Ig, and it targets RBCs Can also see immune thrombocytopenia
27
In a patient with mild symptoms, what does this smear suggest?
This smear shows a bunch of lymphocytes Chronic Lymphocytic Leukemia (CLL)
28
In a patient with mild symptoms, what does this bone marrow aspirate suggest?
Loss of heterogeneity (pea soup) This is a CLL patient
29
What is the classic flow cytometry finding in CLL patients?
See co-expression of CD5 and CD23 See monoclonal B cells - so ALL kappa OR lambda chains. Weak sIgM or IgM/IgD+
30
What is the Rai classification?
Used to stage CLL specifically Stage 0: Lymphocytosis only Stage 1: Lymphadenopathy Stage 2: Splenomegaly Stage 3: Anemia Stage 4: Thrombocytopenia L-LSAT. Rememer that lymphocytosis is always early.
31
How is CLL treated? Who receives treatment?
CLL is not a curable disease. Don't treat patients in early stages of disease because it has no effect on their outcome. Most patients with early stage CLL have a good long-term prognosis.
32
AML is a malignancy of a _______ cell
committed myeloid progenitor cell
33
In AML, the malignant cells largely lose the ability to \_\_\_\_\_
differentiate Reuslts in a morphologically homogenous population of myeloblasts
34
AML is characterized by a clonal expansion of \_\_\_\_
myeloid blasts
35
What classifies a leukemia as AML?
Have \>20% of blood or bone marrow **blasts** **Auer rods** are seen in a subset of cases
36
How do patients develop AML?
Can arise de novo or as a consequence of underlying disorder (like MDS or MPD)
37
Auer rods immediately point to a diagnosis of:
AML
38
Compare/diagnose these two bone marrow biopsies:
Left: This is AML. See a monotonous population of mononuclear cells. Pea soup. Right: This is CML. Still see maturing granulocytes - almost looks normal from afar.
39
What are the clinical manifestations of AML?
Severe anemia Severe neotropenia - causes infections Severe thrombocytopenia Hyperleukocytosis (can cause symptoms of mental status changes, dyspnea with bilateral infiltrates, etc.) - more common with AML Can result in acute DIC (most common in APL)
40
\_\_\_\_ ___ leukemia, specifically the subset \_\_\_, can progress to DIC
Acute myeloid leukemia, specifically Acute Promyelocytic Leukemia (because the promyelocytes produce a lor of Auer rods)
41
Acute Promyelocytic Leukemia:
A subset of AML caused by t(15;17) This translocation disrupts the RAR receptor, causing the accumulation of promyelocytes. Auer rods Risk for DIC ATRA treatment is super important
42
What determines a patient with AML's prognosis?
Age (old is bad) Cytogenetics - e.g. t(15;17) good, bad if arising from somewhere else, such as MDS or myeloproliferative disorder Treatment - if resulting from prior treatment such as chemo or radiation, this is bad. Associated with deletions of chrom 5 and 7
43
How is AML treated? Who is treated?
This can be curable in some patients! Induction - 7+3 chemotherapy. (7 days of cytarabine, 3 days of anthracycline) Consider allogenic stem cell transplant in first complete remission for high risk disease
44
Is CD34 marker associated with AML?
NO - cells are arrested before this! The cells are still blasts.
45
How is APL treated?
Induction chemo WITH **ATRA** (all trans retinoic acid). Also give ARSENIC. ATRA allows the cells to differentiate Stem cell transplant if relapsed
46
Approximately \_\_% of AMLs have no clonal cytogenic abnormality. Instead, characterized by molecular abnormalities such as \_\_\_\_.
50% Mutations at molecular level, such as FLT3 Associated with poor prognosis. Most frequent molecular abnormality in AML. FMS-like Tyrosine Kinase 3
47
ALL is a malignancy of a _____ cell
committed lymphoid progenitor cell (pre-T or B cell)
48
In ALL, the malignant cells largely lose the ability to \_\_\_\_
differentiate
49
Risk factors for ALL development:
MOST COMMON CANCER IN CHILDREN (esp. age 2-5) Risk factors - prior radiation, prior chemo, and familial syndromes like Down Syndrome
50
What is the most common cancer in children?
ALL
51
Does ALL usually arise in B or T cells? Which has a better prognosis? What populations are the common in?
Most commonly in B cells: * B-ALL * Variable prognosis but generally good (better in kids than adults) Less commonly in T cell * T-ALL * Mediastinal or soft tissue mass * Higher risk * Prognosis worse than B-ALL
52
What are the clinical manifestations of ALL?
Severe anemia Severe neutropenia Severe thrombocytopenia Hepatosplenomegaly Tumor lysis syndrome Lymph node involvement (less in AML) Mediastinal mass CNS and testes involvement (need intrathecal chemo to prevent)
53
What predicts the prognosis of ALL patients?
Age: Less than 1 or greater than 10 = bad Cytogenetics: * Good: * t(12;21) * Hyperploidy * Bad: * t(9;22) * 11q23 (MLL) translocations * t(4;11) High white count (\>50 bad) "REMEMBER THESE!!"
54
What diagnosis is indicated by this bone marrow aspirate?
ALL
55
What is the key marker for a lymphoblast?
TdT+ (this is a DNA polymerase)
56
What is the key marker for a myeloblast?
myeloperoxidase (can crystallize into an Auer rod)
57
What markers are commonly used to check for ALL?
CD19+ CD10+ TdT+ No surface light chain
58
Favorable ALL prognoses are associated with a translocation of ____ and ____ ploidy. Intermediate prognoses are associated with translocation \_\_\_. UNfavorable prognoses are associated with a translocation of ___ and mutation \_\_\_\_, with ___ ploidy.
Favorable ALL prognoses are associated with a translocation of **t(12;21)** and **hyperdiploid** ploidy. Intermediate prognoses are associated with translocation **t(1;19)**. UNfavorable prognoses are associated with a translocation of **t(9;22)** and mutation **abn(11q23)**, with **hyplodiploid** ploidy.
59
A 75-year-old patient with CLL is asymptomatic and no significant lymphadenopathy, splenomegaly, or cytopenias. What is the most reasonable next step for this patient?
Watchful waiting. Don't benefit from treatment at early stages.

Hematology Block 3 (8 decks)

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