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Heme/Lymph 1 CP > 4- Introduction to WBC Disorders Reactive an Neoplastic Myeloid Processes Targeted Leukemia Therapy > Flashcards

4- Introduction to WBC Disorders Reactive an Neoplastic Myeloid Processes Targeted Leukemia Therapy Flashcards

1
Q

In order to make a diagnosis of acute leukemia, how many blasts (at a minimum) would you have to se in a peripheral blood (or bone marrow) smear?

A

over 20%

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2
Q

What cells are these?

A

Neutrophils! You rock!

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3
Q

What type of WBC would be elevated with a streptococcal tonsilitis infection? How about Mono? Whooping cough? Cutaneous larva migrans? G-CSF administration?

A

mono- lymphocytes

strep tonsilitis- neutrophils

whooping cough- lymphocytes

cutaneous larva migrans- eosinophils

G-CSF- neutrophils (but not as elevated as with a bacterial infection)

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4
Q

What would the following laboratory tests be used to confirm?

JAK2 mutational analysis

Throat culture

Monospot test

Cytogenetics for the philadelphia chromosome

flow cytometry for Tdt(+) cells

A

JAK2 mutational analysis- PV, ET, PMF

Throat culture: Strep tonsilitis (neutrocytoses)

Monospot test: Infectious mononucleosis

Cytogenetics for the philadelphia chromosome: CML

flow cytometry for Tdt(+) cells: ALL (notice this is not the word all, I was confused at first haha)

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5
Q

What is the significance of “toxic changes” in peripheral blood neutrophils?

A

indicates the presence of primary granules

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6
Q

What disease is associated with Disseminated Intravascular Coagulation (DIC) and has the following histology?

A

Acute Myeloid Leukemia

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7
Q

Which cytogenic abnormality is associated with the following histology slide?

A

t(15;17)

There are a LOT of Auer rods so it is probably APL

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8
Q

What is the funcional defect that is associated with the product of the PML-RARa fusion gene? Therefore what therapy is recommended?

A

A block in terminal differentiation due to retinoic acid receptor disruption

therapy is all trans retinoic acid

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9
Q

Which cytogenic/molecular abnormalities have a similar prognostic significance to t(15;17), in a patient with AML?

A

t(8;21)

inv(16) aka t(16;16)

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10
Q

Leukemias are about 5% of all cancers. (S/O to Miss Matter). WHat percentage of adult leukemias are Acute Myelogenous Leukemia? What percentage of their etiologies re therapy related?

A

AML is 30% of adult leukemias and 10% of them are due to therapy

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11
Q

What 3 things does the prognosis of AML depend on?

A

Age

cytogenetics

Molecular

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12
Q

What is the difference bewteen cytogenetics and Molecular?

A

Cytogenetics is BIG, like a peice of highway compeltely dropped off

MOlecular is SMALL, like a little pot hole in the road (usually point mutations)

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13
Q

WHat does induction mean? And what drugs are usually used furing the induction process for AML?

A

Induction is inducing the patient into remission!

“7+3” with Ara-C + Daunorubicin

+Midostaurin (with FLT3 mutation)

Mylotarg (with CBF mutation) (immunotherapy)

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14
Q

What is consolidation?

A

Consolidation is ensuring that the patient is in remission!

chemotherapy

or stem cell transplantation

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15
Q

WHat does this patent likely have and why?

A

Chronic myelogenous leukemia

  • blasts are <20% so not acute
  • leukocytoses
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16
Q

In MDS would you have leukocytoses or leukopenia?

A

Leukopenia

17
Q

Hypercellular bone marrow with effective hematopoiesis is seen in what?

A

Myeloproliferative Neoplasms (PV, ET, PMF, CML)

18
Q

What are the basic questions you should ask yourself to assess what disease a person has, and then also to assess its severity?

A
  • Are blasts>20%
    • if yes, its acute= emergency
      • AML or ALL
    • if no, chronic= not emergency
  • What cells are elevated?
19
Q

WHat is hypercellular bone marrow with ineffective hematopoiesis associated with?

A

MDS

20
Q

What is Hypercellular bone mrrow with extensive fibrosis associated with?

A

PMF

21
Q

Leukocytes positive for CD10 is associated with what?

A

ALL

22
Q

Leukocytes positive for JAK2V617F mutation suggestive of?

A

MPN :PV, EET, PMF

Not CML bc that is tyrosine kinase

23
Q

What protein does the Philadelphia result in and what is the translocation?

A

The philadelphia chromosome, which brings about the BCR-ABL fusion protein is the consequence of t(9;22)

24
Q

WHat is the functional defect that is associated with the product of the BCR-ABL fusion gene? What therapy is often used?

A

A constitutively activated tyrsine kinase

A tyrosine kinase inhibitor is recommended for CML

25
Q

What is Chronic Myelogenous Leukemia (CML)? What are 2 hallmarks? Etiologies?

A
  • Clonal myeloproliferative disorder of pluripotent stem cells. Increased proliferation and decreased apoptosis
  • Hallmarks:
    • Cytogenetic- Philidephia chromosome
    • Molecular-BCR/ABL
  • Etiology: Irradiation <5%, Unkown 95%
26
Q

What are the 3 phases of CML progression without treatment?

A

Chronic

Accelerated

Blast phase

without treatment people usually go through all the phases and die within 7 years

27
Q

How does a tyrosine kinase inhibitor work? When do we use it?

A

Typically ATP binds to BCR ABL

A TKI blocks the ATP binding sit so ATP can’t bind

No proliferation, Cell dies

**Used for CML!

28
Q

What are 5 TKIs? How effective are these?

A

Imatinib

Dasatinib

Nilotinib

Bosutinib

Ponatinib

The lifespan of people on this drug are about the same as a person without CML! Unfortunately the side effects are brutal so even though a person’s survival is preserved, their quality of life is not

29
Q

A patient has elevated hemoglobin and platelets, and a JAK2 mutational analysis is homozygous for the V617F mutation. What lab finding is likely present?

A

Decreased EPO

This patient probably has PV

30
Q

A patient has elevated hemoglobin and a spleen palpable 4cm at MCL presenting with fatigue, cachexia, bone pain, night sweats and the following histology. What lab test would be positive to confirm the diagnosis?

A

JAK2 mutational analysis. This is PMF!

31
Q

What are the 4 MPNs? What mutations typically cause them?

A

Polycythemia vera (JAK2)

Essential thrombocythemia (JAK2)

Primary myelofibrosis (JAK2)

Chronic Myeologenois leukemia (Tyrosine kinase)

32
Q

A patient presents with pancytopenia, hyperceullar bone marrow, and frequent hypogranular and hypolobated neutrophils, and small, hypolobated megakaryocytes. What is the most likely diagnosis?

A

Myelodysplastic syndrome

MDS- Pancytopenia (ineffective hematopeiesis) and hypercellular bone marrow

33
Q

What is the most important diagnostic criterion in differentiating myelodysplastic syndrome from and acute myeloid leukemia with myelodysplasia-associated changes?

A

Bone marrow blast percentage! in AML blast>20%

34
Q
A
35
Q

What cytogenic abnormality is most likely to be found in a patient with MDS? What is the most likely treatment?

A

Monosomy 7

A hypomethylating agent

36
Q

What are the therapies for myelodysplastic syndrome?

A

Stem cell transplantation (BM transplant)

Supportive care +/- growth factors

hypomethylating agents

lenalidomide

histone deacetylase inhibitors

37
Q

What is the Molecular mechanism for MDS? How do the therapies interfere with this?

A

Hypermethylation of genes silences them blocking gene expression leading to a differentiation problem (MDS)

Hypomethylating agents work by preventing DNAmethytransferase from hypermethylating

38
Q

How do hypomethylating agents help with lifespan of patients with MDS?

A

9.4 months

39
Q

What are the 3 categories of leukemias? Which ones fall into each category?

A
  • Problems with Differentiation
    • MDS
  • Problems with Proliferation
    • CML and /CLL
    • PV
    • ET
    • PMF
  • Problems with BOTH DIfferentiation and proliferation
    • AML and ALL

Heme/Lymph 1 CP (12 decks)

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