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Hematology > Leukemia > Flashcards

Leukemia Flashcards

1
Q

Describe acute leukemias in general terms

A

cancers of the hematopoeitic progenitor cells

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2
Q

Describe chronic leukemias in general terms

A

cancers involving proliferation of more fully differentiated myeloid and lymphoid cells

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3
Q

What is myelogenous leukemia?

A

characterized by proliferation of myeloid tissue (as of the bone marrow and spleen) and an abnormal increase in the number of granulocytes, myelocytes, and myeloblasts in the circulating blood

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4
Q

What are lymphocytic leukemias?

A

characterized by immature lymphocytes and their progenitors that originate in the bone marrow, but infiltrate the spleen, lymph nodes, CNS, and other tissues.

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5
Q

What are the 3 purposes of combination chemotherapy?

A

decrease drug resistance, decrease drug toxicity to the patient by using multiple drugs w/varying toxicities, and interrupt cell growth at multiple points in the cell cycle

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6
Q

What is induction therapy?

A

high-dose therapy used before bone marrow transplant

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7
Q

What is consolidation/intensification therapy?

A

May be given after induction therapy. Purpose is to eliminate remaining leukemic cells that may not be evident

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8
Q

How does bone marrow and stem cell transplantation work?

A

Eradicates patient’s hematopoietic stem cells and

replaced with those of an HLA-matched (Human Leukocyte Antigen), MLC (mixed Leukocyte Culture) donor

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9
Q

What is AML?

A

neoplasms affecting myeloid precursor cells in the bone marrow. normal cells are replaced by undifferentiated blast cells leading to anemia, neutropenia, thrombocytopenia

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10
Q

What are risk factors for AML?

A

age > 60, benzene or radiation exposure, tobacco, down syndrome, previous breast/ovarian ca or lymphma

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11
Q

What laboratory and radiographic work-up should you do for AML?

A

CBC with manual differential, Uric Acid level, Clotting studies (PT, PTT, D-dimer, fibrinogen), Bone marrow aspirate and biopsy

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12
Q

What are hematological findings for AML?

A

Anemia (normochromic, normocytic), Leukocytosis (median = 15,000), Thrombocytopenia (< 100,000)

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13
Q

What morphology and cytology changes do you see with AML?

A

> 20% myeloblasts in blood and/or bone marrow, Auer Rods (cytoplasmic granules), hypercellular bone marrow

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14
Q

What are the treatments for AML?

A

Chemotherapy: Phase One – Induction therapy. Phase Two – Intensification therapy. Phase Three – Maintenance. Radiation therapy for certain cases. Bone marrow transplantation

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15
Q

What are complications of AML treatment?

A

Anemia, Infection, Bleeding, Metabolic abnormalities, Ocular, Venous thromboembolus

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16
Q

What is the prognosis for AML?

A

Five year survival rate in adults under 65 is 33%. Five year survival rate in adults >65 is 4%

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17
Q

What is ALL?

A

Clonal proliferation and accumulation of blast cells in blood, bone marrow and other organs. Disorder originates in single B or T lymphocyte progenitor

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18
Q

What is proposed etiologies of ALL?

A

Genetic - Philadelphia chromosome, Viral infection (EBV, HIV), Exposure to high energy radiation (T-cell ALL), Toxic chemical exposure

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19
Q

What is laboratory and radiographic work-up for ALL?

A

CBC with manual differential, Chemistry studies to check for organ dysfunction, Bone marrow aspirate and biopsy Genetic/Immunological studies, Lumbar puncture

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20
Q

What are hematological findings associated with ALL?

A

Anemia (normochromic, normocytic), WBC < 5,000 (or > 25,000), Leukocytosis (median = 15,000), Thrombocytopenia, Smear-Blast cells

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21
Q

What do you need in order to do ALL staging?

A

Bone marrow biopsy, Cytogenic studies, Lumbar puncture, CT scans

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22
Q

What does the treatment strategy for ALL depend on?

A
  1. Risk qualification 2. Immunophenotype of leukemic cells- T lineage, early B lineage, mature B lineage 3. Age and biological condition
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23
Q

What classifies someone as high risk ALL?

A

Age > 35 years, WBC > 30 G/L in B-ALL, > 100 G/L in T-ALL. No remission after 4 weeks of induction therapy

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24
Q

What classifies someone as very high risk ALL?

A

Chromosome Philadelphia - positive or BCR/ABL(+)

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25
Q

What is treatment strategy for ALL?

A

Induction/CNS Prophylaxis, Consolidation/intensification, Maintenance

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26
Q

What is included in remission induction therapy in ALL?

A
  1. Antineoplastic treatment- Drugs: prednisone, vincristine, asparginase, cyclophosphamide, duanorubicin/adriablastin/epirubicin, cytosine arabinoside, 2. CNS preventative tx 3. Supportive care 4. Treatment of complications
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27
Q

What are induction treatment complications?

A

Tumor lysis syndrome, Thrombosis, Bleeding, Infection, Anaphylaxis, HPA axis suppression

28
Q

What is maintenance therapy in standard risk ALL?

A

low dose chemo: 6-mercaptopurine, methotrexate - for 2-3 years. Intensification treatment periodically repeated: daunorubicin/adriablastin, prednisone, vincristine, cyclophosphamide.

29
Q

What is the consolidation therapy in high-risk ALL?

A

. Intensification treatment: amsacrine, mitoxantrone, idarubicine, high dose cytosine arabinoside, high dose methotrexate, high dose cyclophosphamide.Hematopoietic stem cell transplantation - high-dose therapy or reduced intencity conditioning

30
Q

What is the consolidation therapy in very high risk ALL?

A

High-dose therapy (reduced-intensity ?) + allogeneic stem cell transplantation

31
Q

What is prognosis for ALL?

A

Children-Complete remission (CR) 95-99%, Leukemia-free survival (LFS) ~80%. Adults Complete remission (CR) 80-85% Leukemia-free survival (LFS) 30-40%

32
Q

What is CML?

A

Proliferative disorder of hematopoietic stem cells

characterized by proliferation of marrow granulocytes, erythroid precursors, and megakaryocytes.

33
Q

CML is associated with what chromosomal abnormality?

A

Philadelphia (Ph) chromosome

34
Q

CML is associated with what molecular abnormality?

A

Bcr-Abl tyrosine kinase

35
Q

What happens as a result of the philadelphia chromosome transloction?

A

the fusion of BCR-ABL possesses tyrosine kinase activity that lets cells bypass cell growth regulators resulting in malignant transformations.

36
Q

What is the Philadelphia (Ph) chromosome

A

Reciprocal translocation of chromosome 22 and chromosome 9. The portion of chromosome 9 contains ABL and it’s received at the BCR site of chromo 22. 90-95% of CML pts have it

37
Q

What are the phases of CML?

A

Chronic Phase, Accelerated Phase, Blast Crisis

38
Q

What are the chronic phase CML clinical features?

A

40% asymptomatic. Splenomegaly often massive increasing the abdominal girth

39
Q

What are CML clinical features?

A

Pallor, dyspnea, tachycardia, Bruising, epistaxis, menorrhagia, Hyperleukocytosis, thrombosis, gout, Visual disturbances, Chronic infection, Fever

40
Q

How should you work-up CML?

A

CBC with manual differential. Serum Vitamin B12 and B12 binding capacity. Leukocyte alkaline phosphatase (decreased). Uric acid level. Chromosomal testing - Philadelphia chromosome. Bone marrow biopsy

41
Q

What are expected hematological findings of CML?

A

Anemia (normochromic, normocytic). Leukocytosis (median = 20,000). Basophilia. Thrombocytopenia

42
Q

CML Bone Marrow features

A

Hypercellular. Myeloid:erythroid ratio – 10:1 to 30:1.
Myelocyte predominant cell, blasts less 10%. Megakaryocytes increased & dysplastic. Increase reticulin fibrosis to 30-40%

43
Q

Describe the Chronic phase of CML?

A

3-5 years. Current treatment is with alpha-interferon. Young patients should undergo BMT.

44
Q

Describe the accelerated phase of CML?

A

Difficult to control, lasts 6-9 months. Splenomegaly and increasing chemo requirements. Hypermetabolism sx. Lab: blasts >15%, blast and promyelocyte > 30%, basophil > 20%, thrombocytopenia.

45
Q

Blast phase

A

> 30% blasts in blood or marrow. Similar to acute leukemia. 2/3 transform to myeloid blastic phase and 1/3 to lymphoid blastic phase. Survival : 3-6 mos

46
Q

What are CML treatments to control and prolong chronic phase (non-curative)?

A

-Imatinib mesylate (Gleevec) or other small molecule therapy, Alpha interferon (IFN-), chemotherapy (Hydroxyurea)

47
Q

What are CML treatments to eradicate malignant clone (curative) in the chronic phase?

A

Imatinib mesylate (Gleevec). Thyrosine kinase inhibitor. Allogeneic transplantation. Alpha interferon

48
Q

What is the CML prognosis?

A

Median survival 3.5 yrs (range 2-8 yrs). Interferon + chemotherapy :6 years. Transplant : 5+ years. Imatinib mesylate (Gleevec)80% survival – 9 years

49
Q

What is the most common lymphoid leukemia?

A

CLL which is a clonal malignancy of B lymphocytes

50
Q

CLL Epidemiology

A

Median age at diagnosis is 70 years. Males > Females. Hallmark is isolated lymphocytosis

51
Q

What is the proposed etiology of CLL?

A

Genetic, Viral infection (EBV, HIV) - Burkitt’s Lymphoma, Exposure to high energy radiation (T-cell ALL), Toxic chemical exposure, Smoking

52
Q

What are symptoms of CLL?

A

Fever, Night sweats, Fatigue, Pallor, Shortness of breath, Easy bruising, Gingival bleeding, Weight loss, Frequent infections

53
Q

CLL physical findings

A

Splenomegaly and/or hepatomegaly, Lymphadenopathy, Multiple bruises, Bleeding gingivae, Leukemia cutis

54
Q

How should you work-up CLL?

A

CBC with manual differential, Peripheral smear

Chemistry studies to check for organ dysfunction, Flow cytometry, Lymph node biopsy

55
Q

What is the diagnostic criteria for CLL?

A

lymphocyte count > 20,000/microL, usually 75-98% lymphocytes. HCT & platelets are normal. bone marrow aspirates showing >30% smudge cells. The cell should have the presence of B-cell specific differentiation antigens

56
Q

Pretreatment studies of patients with CLL should include examination of:

A

CBC, peripheral blood smear, reticulocyte count, Coomb’s test, renal and liver fxn tests, serum protein electrophoresis, immunoglobulin levels, plasma 2 microglobulin level, immunophenotyping, CXR

57
Q

What are treatment options for CLL?

A

Alkylating agents (chlorambucil, cyclophosphamide). Nucleoside analogs (cladribine, fludarabine). Biological response modifiers. Monoclonal antibodies. Bone marrow transplantation

58
Q

Describe Hairy Cell Leukemia

A

2% of all adult leukemias. Usually in males > 40 years old. Chronic disease of lymphoproliferation B lymphocytes that infiltrate the bone marrow and liver

59
Q

Hairy Cell Leukemia Clinical presentations

A

Splenomegaly, Pancytopenia, Infection, Vasculitis

60
Q

What labs should be done w/hairy cell leukemia?

A

CBC, Liver function tests, Kidney functions

61
Q

What does Hairy Cell Leukemia treatment consist of?

A

Chemo-alpha-interferon, pentostatin, cladribine

62
Q

Rai Classification for CLL

A
  1. Lymphocytosis (>5 G/L)
  2. Lymphocytosis + lymphadenopathy
  3. Lymphocytosis + splenomegaly +/-lymphadenopathy
  4. Lymphocytosis + anemia (Hb <100G/L) +/- anemia +/-lymphadenopathy +/- splenomegaly
63
Q

Binet Classification for CLL

A

A. < 3 involved areas, Hb > 10g%, Plt > 100G/L
B. > 3 involved areas, Hb > 10g%, Plt > 100G/L
C. Any number of involved areas, Hb < 10g%,
Plt < 100G/L

64
Q

Name a tyrosine kinase inhibitor and what it is used to treat

A

imatinib mesylate. treats leukemias that display the philadelphia chromosome translocation (CML)

65
Q

What are the shared clinical features of ALL and AML?

A

fatigue, fever, night sweats, weight loss, bleeding, bone pain and tenderness, infections. lymphadenopathy, splenomegaly, hepatomegaly are more common in ALL, but still occurs in AML.

66
Q

What differentiates ALL from AML clinically?

A

CNS involvement is more common with ALL: nerve palsies, HA, N/V, papilledema

67
Q

What can cause hyperuricemia and how is it treated?

A

occurs as a result of increased proliferation or increased breakdown of purines secondary to leukemic cell death. Treat w/allopurinol which inhibits uric acid synthesis.

Hematology (16 decks)

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