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Adult/Ped Med 7- Grant's > Adult Leukemias > Flashcards

Adult Leukemias Flashcards

1
Q

When you have an abnormality i the blood cells that causes either uncontrollable proliferation, or stops cell regulated cell death, it is called…

A

Leukemia. Characterized by growth (Acute=fast, Chronic=slow) and type of cell affected.

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2
Q

What is not normal on a peripheral smear?

A

Blasts- REFER!

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3
Q

Erythrocytes, megakaryocytes, monocytes, and granulocytes come from what stem cell lineage?

A

Myeloid. T lymphocyte, NK Lymphocyte, and B lymphocyte come from lymphoid stem cell.

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4
Q

Most common pediatric cancer

A

Acute lymphocytic leukemia (ALL)

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5
Q

T/F: Most Adults with ALL are cured while children relapse?

A

False: Switch

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6
Q

Presenting signs/symptoms of ALL

A
  • Bone marrow failure- Anemiam Thrombocytopenia, neutropenia

- Leukemic infiltration- Bone pain, HA, organomegaly, neurologic symptoms, lymphadenopathy

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7
Q

Diagnostics for ALL

A
  • CBC with manual diff
  • Tumor lysis labs
  • Coags
  • CXR/CT
  • Bone marrow aspirate
  • Spinal tap
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8
Q

ALL is characterized by the uncontrolled proliferation of ________. This limits the production of other cells by overcrowding and inhibits cell growth and differentiation.

A

Lymphoblasts

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9
Q

Most common type of cell in ALL

A

Precursor B-Cell

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10
Q

Burkit-cell leukemia and frequently occurs in HIV patients involves what cell line

A

Mature B cell

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11
Q

A poor prognosis and associated with HTLV-1 infection. WHat type of cell in ALL?

A

T-cell

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12
Q

3 phases in ALL treatment

A

1) Induction- includes vincristine, CCS, anthracycline
2) Post-remission consolidation- rotational consolodation, stem cell transplant
3) Maintenance therapy: Includes Methotrexate, 6-mercaptopurine

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13
Q

ALL: Prognostic factors

A
  • Age
  • Leukocyte count at presentation
  • Time to achieve CR
  • Immunophenotype
  • Cytogenic abnormalities
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14
Q

A High WBC at presentation in AML means what?

A

Poor prognostic factor- WBC100k association with induction death

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15
Q

Treatment of choice for ALL

A

Bone marrow transplant

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16
Q

T/F: The incidence of AML is 5X greater than ALL

A

True

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17
Q

Describe the clinical presentation of AML

A

Abrupt onset (1-6 month prodromal period)

  • Similar symptoms to ALL- fatigue, flulike, bleeding, petechiae, purpura, gingival bleeding, GI bleeding, urinary tract bleeding due to decreased platelets.
  • Increased susceptibility to infections due to neutropenia
  • Enlarged spleen
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18
Q

Detection and Dx for AML

A
  • Blood counts, abnormal blood counts lead to detection of AML: Thrombocytopenia, anemia, increased leukocytes.
  • Chromosomal abnormalities
  • Presence of Auer rods (structres found in myeloblasts, myelocytes, and monoblasts)
  • Bone marrow aspiration biopsy for definitive diagnosis.
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19
Q

True/False: If 30% blast cells are present, acute leukemia is confirmed?

A

True- DDX is made from staining procedure. Immunophenotyping as in ALL establishes diagnosis in 90% of cases.

20
Q

Pathology of AML

A
  • Proliferation of precursor cells that have lost the ability to differentiate.
  • It involved the hematopoietic stem cells or pluripotent cells
  • Results in the gradual accumulation of undifferentiated cells in marrow or other organs.
21
Q

French-American-British Classification of AML

A 
M0- Undifferentiated (MPO negative)
M1- Without maturation
M2- With granulocytic maturation
M3- Acute promyelocytic
M4- Myelomonocytic
M5- Monocytic
M6- Erythroleukemia
M7- Magakaryoblastic
22
Q

Treatment of AML

A
  • Intensive Chemo: Induction, consolidation

- Stem cell transplant

23
Q

A distinct clinical and biologic subtype of AML.

  • The most curable AML.
  • Separate treatment algorithim from other AML subtypes
  • T (15:17) results in fusion transcription gene (PML-RAR a)

WHAT IS IT?

A

Acute Promyelocytic leukemia (APL)

24
Q

T/F: AML M3 is initially treated differently?

A

True

25
Q

T/F: Cytogenetics provides critical prognostic info but it is not used to dictate treatment.

A

False- It now dictates treatment

26
Q

T/F: Chronic Leukemias is the overproduction of blood cells, may not need immediate treatment, and is sometimes found on routine health care maintenance?

A

True

27
Q

What is the most common leukemia?

A 
CLL
-Accounts for 30% of leukemias
-CLL 2X as common as CML
-Incidence increases with age, rare under 35
Males more common.
28
Q

Clinical presentation of CLL

A
  • Usually asymptomatic
  • Bruising (thrombocytopenia)
  • Early satiety (splenomegaly (late))
  • Recurrent infections
  • Lymphadenopathy
29
Q

T/F: Male sex, White ancestry and Family hx are risk factors for CLL

A

True

30
Q

CLL Lab Findings:

A
  • Lymphocytosis: NO blasts!! All mature lymphocytes.
  • Hypogammaglobinemia
  • Smudge cells
31
Q

CLL Work Up includes

A
  • Adequate Hx/physical
  • CBC, Differential, PLT count
  • CMET, LDH, B2-microglobulin
  • Occasionally: Direct coombs, bone marrow aspirate/biopsy, serum immunoglobulins
  • Retic count
  • CXR/abdominal/pelvic
  • Flow cytometry
  • Cytogenetics
  • Molecular studies-Ig receptor gene rearrangements
32
Q

CLL Staging: Rai Staging System

A
  • Low (0)= Lymphocytosis in PB and BM
  • Intermediate (I-II)= Lymphocytosis, lymphadenopathy, hepatosplenomegaly
  • High (III-IV)= Lymphocytosis, anemia, thrombocytopenia
33
Q

CLL Staging: Binet Staging

A 
A= HGB >10, PLT>100K, 10, PLT>100k, 3 or more nodal areas involved
C= HGB ,10, PLT<100K, or both, independent of nodal ares involved
34
Q

T/F:

1) CLL is traditionally an illness of younger individuals?
2) CLL well patients do not require therapy?
3) IVIG monthly replacement if hx of bacterial infections (management not treatment)?
4) Earlier/ more aggressive conventional therapy has shown to improve survival or cure of patients?

A

1) False- older pts
2) True
3) True
4) False: not clearly known to improve

35
Q

Initial therapies in treatment of CLL include:

A
  • Oral chemo
  • Single agent IV chemo
  • Combo therapy
  • Campath-monoclonal antibody
36
Q

What is this: Accounts for 20-30% of all leukemias. Rare in children. Uncommon before age 21. Peaks in 40s. Males slightly more common.

A

CML

37
Q

The etiology of CML is unknown. Maybe linked to radiation, benzene? What chrmosome is present in 95% of CML patients.

A

Philadelphia chromosome. Abnormal Ch 22- loss of part of long arm.

38
Q

What are prognostic indicators dependent on in CML?

A
  • Spleen size
  • PLT count
  • Hematocrit (% of erythrocytes in blood volume)
  • Gender
  • % of blood myeloblasts (immature BM cells)
39
Q

What phase of CML is this: Median survival of 3.5-5 years before transformation. Asymptomatic in 15-40%. May have abdominal complaints/exam consistent with organomegaly.

A

Chronic phase

40
Q

What phase of CML is this: Median survival 18 months. Peripheral blasts >15%. Increased basophils. Difficult to control white count. Thromocytopenia. Patient with more symptoms such as fever, night sweats, and wt. loss.

A

Accelerated phase

41
Q

What phase of CML is this? Equivalent to AML. Median survival 3-6 months. Signs include peripheral blasts >30%, marrow blasts >30%, clumps of blasts on BM bx, extramedullary chloromas. Symptoms are similar to accelerated phase.

A

Blast crisis

42
Q

Lab findings in CML include:

A
  • Leukocytosis

- Thrombocytosis (Sometimes over 1mil.)

43
Q

CML Diagnostic test:

A

Peripheral blood or bone marrow

-Philadelphia chromosome- translocation (9;22). Involves bcr/abl. Tested by FISH cytogenetics

44
Q

How would you treat stable CML?

A

Gleevec- tyrosine kinase inhibitor

45
Q

How would you treat unstable CML?

A
  • Admission to control counts- Leukapheresis, hydrea, blast crisis treat as AML.
  • Medication failures: Stem cell transplant
46
Q

What is this: A malignant tumor of myeloid cells. Can be found in kidney, skin, brain, bowel, etc. Solid tumor may be only sight of disease (bone marrow clear). Still treat systemically.

A

Granulocytic Sarcoma

47
Q

The take home message with acute leukemia is to not mess around. This means you should…

A

REFER!

Adult/Ped Med 7- Grant's (10 decks)

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