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Heme/Oncology > hematologic malignancies > Flashcards

hematologic malignancies Flashcards

1
Q

blood cancer

A

myelodysplastic syndrome

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2
Q

consist of a group of acquired clonal neoplasms of the hematopoietic stem cell

characterized by:
- constellation of cytopenias
- hypercellular marrow
- morphologic dysplasia
- genetic abnormalities

A

myelodysplastic syndrome (MDS)

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3
Q
  • > 60 years old
  • asymptomatic when diagnosis made (incidental finding of abnormal blood counts)
  • cytopenia (fatigue, infection, bleeding)
  • on exam: splenomegaly, pallor, bleeding, infection
A

myelodysplastic syndrome (MDS) signs and symptoms

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4
Q

CBC:
- anemia with normal or increased MCV
- left shift (immature neutrophils)

peripheral blood smear:
- macro ovalocytes (RBCs)
- neutrophils with morphologic abnormalities

A

myelodysplastic syndrome (MDS) lab findings

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5
Q

what do you see on bone marrow aspiration/biopsy of MDS

A
  • hypercellular
  • erythroid hyperplasia
  • signs of abnormal erythopoeisis
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6
Q

what do you see on bone marrow aspiration/biopsy of MDS (Prussian blue stain)

A

ringed sideroblasts

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7
Q

what do you see on bone marrow aspiration/biopsy of MDS (in the marrow)

A

myeloid series often left shifted, with variable increases in blasts

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8
Q

what do you see on bone marrow aspiration/biopsy of MDS (characteristic abnormality)

A

dwarf megakaryocytes with unilobed nucleus

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9
Q

what defines MDS

A
  • genetic abnormalities
  • frequent cryogenic abnormalities involving chromosome 5 and 7
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10
Q

how to differentiate between myelodysplasia and AML

A

as the number of blasts increase in bone marrow, myelodysplasia has <20% blasts

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11
Q

low risk MDS treatment

A

improve blood clots
- erythropoietic growth factors

chromosomal abnormality
- lenalidomide

immunosuppressive therapy
- anti-thymocyte globulin

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12
Q

high risk MDS treatment

A

preventing leukemia:
- hypomethylating agents (azacitidine and decitabine)
- bone marrow stem cell transplant (only cure)

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13
Q

Arise from the lineage that gives rise to granulocytes (neutrophils, eosinophils, basophils, and
monocytes), erythrocytes, and platelets

A

Myelogenous leukemias (AML and CML)

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14
Q

Involve the lymphocytic lineage (that gives rise to T and B lymphocytes

A

Lymphocytic leukemias (ALL and CLL)

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15
Q

cancer found in the blood and bone marrow, caused by too many white blood cells in the body. the white blood cells don’t let the body fight disease and prevent the body from making red blood cells and platelets.

A

leukemia

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16
Q

there are lots of partially developed WBC in the blood over a long
period of time

These partially developed WBC interfere with the development and function of healthy
WBC, platelets, and red blood cells

A

chronic leukemia

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16
Q

Myeloproliferative disorder characterized by overproduction of myeloid cells

A

chronic myeloid leukemia (CML)

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17
Q

hallmark of chronic myeloid leukemia

A

philadelphia chromosomes also called fusion gene (bcr/abl)

detected by PCR testing of the peripheral blood and bone marrow

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18
Q

translocation between long arms of chromosome 9 and 22

A

philadelphia chromosomes

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19
Q

produces a protein that
possesses tyrosine kinase activity

Leads to excessive proliferation and reduced
apoptosis of CML cells

induces leukemia in hematopoietic
cells

A

fusion gene (bcr/abl)

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20
Q

(90% of time at diagnosis)

Early CML

Does not behave like a malignant disease
* Normal bone marrow function is retained
* WBCs differentiate
* Neutrophils combat infections normally

A

CML chronic phase

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21
Q

Untreated CML can progress to an

A

“acute blast” phase

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22
Q

Disorder of middle age* (median age 55 years)
* Fatigue, night sweats, low-grade fevers
* Abdominal fullness due to splenomegaly*
* Exam: Splenomegaly, sternal tenderness

A

CML signs and symptoms

23
Q

what do you see on peripheral blood smear for CML

A
  • elevated WBC count
  • myeloid series left shifted with mostly mature cells
  • blasts <5%
24
Q

what do you see on bone marrow biopsy for CML (essential to confirm the phase of disease)

A
  • karotype
  • bone marrow is hyper cellular, with left shifted myelopoiesis
25
Q

when is blast phase CML diagnosed

A

when blasts comprise >20% of bone marrow cells

26
Q

extreme hyperleukocytosis CML treatment

A

Emergent leukapheresis with myelosuppressive therapy

27
Q

chronic phase CML treatment

A

tyrosine kinase inhibitor (imatinib)

28
Q

advanced stage disease CML treatment

A
  • tyrosine kinase inhibitor alone or in combo with myelosuppressive therapy
  • consider stem cell transplant
29
Q
  • Malignancy of B lymphocytes
  • Indolent, with slowly progressive accumulation of long-lived small lymphocytes
  • Manifested clinically by:
  • Immunosuppression
  • Bone marrow failure
  • Organ infiltration with lymphocytes
A

chronić lymphocytic leukemia (CLL)

30
Q

Disease of older patients, 90% >50 years and median age of 70 years

  • Incidentally discovered to have lymphocytosis
  • May present with fatigue or lymphadenopathy

Exam:
* 80% will have diffuse lymphadenopathy
* 50% will have enlargement of the liver or spleen

A

signs and symptoms of CLL

31
Q

what is the hallmark of CLL

A

isolated lymphocytosis

32
Q

CLL bone marrow lab findings

A

small lymphocytes
(diagnosis made from phenotype and genetic markers)

33
Q

CLL smudge cells lab findings

A

cell remnants from fragile cells

34
Q

early indolent CLL treatment

A

observation is standard of care

35
Q

what are indication of starting therapy for CLL

A
  • progressive fatigue
  • symptomatic lymphadenopathy
  • anemia
  • thrombocytopenia
36
Q

CLL initial treatment

A

targeted biologic therapy:
- BTK inhibitor as single agent (ibrutinib, acalabrutinib, or zanubrutinib)
- OR venetoclax in combo with anti-CD20 antibody therapy (obinutuzumab)*

37
Q
  • chromosomal translocation
  • philadelphia chromosome
  • myeloid leukocytes (granulocytes and monocytes)
  • stop maturing and divide quickly
  • buildup and hepatosplenomegaly
A

CML

38
Q
  • chromosomal abnormalities
  • interfere with B cell receptors
  • lymphoid leukocytes (B cells)
  • stop maturing and die too slowly
  • buildup and lymphadenopathy
A

CLL

39
Q
  • Malignancy of the hematopoietic progenitor cell
  • Malignant immature cells proliferate in an uncontrolled fashion and replace normal bone marrow
    elements
  • Most cases arise with no clear cause
  • MDS –> AML*
  • Down Syndrome is associated with AML and ALL
A

acute leukemia

40
Q

median age 60 years (MC acute leukemia of adults)*

Malignancy of myeloblasts

A

AML

41
Q

peak incidence 3-7 years (MC childhood leukemia)*
* Malignancy of precursor B or T lymphocytes
* It is also seen in adults- 20% of adult acute keukemias

A

ALL

42
Q
  • Ill for days or weeks
  • Bleeding (due to thrombocytopenia) of skin and mucosal surfaces (gingival bleeding, epistaxis, or menorrhagia)
  • Infection (due to neutropenia) – risk rises as neutrophil count falls <500/mcL
  • Cellulitis, pneumonia, perirectal infections, fungal
  • Gum hypertrophy and bone and joint pain
  • Exam –> pale, purpura, petechiae, stomatitis, gum hypertrophy, rectal fissures, enlargement of liver, spleen and lymph nodes, bone
    tenderness of sternum, tibia and femur
A

signs and symptoms of acute leukemia

43
Q
  • Hallmark of acute leukemia is combination of pancytopenia with circulating blasts
  • Bone marrow is usually hypercellular and dominated by blasts (>20%)
  • Hyperuricemia
  • ALL (especially T cell)– mediastinal mass visible on CXR
  • Auer rod (eosinophilic needle-like inclusion in the cytoplasm)- characteristic of AML
A

acute leukemia lab findings

44
Q

hallmark of acute leukemia

A

pancytopenia with circulating blasts

45
Q

characteristic of AML

A

auer rod (eosinophilic needle like inclusion in the cytoplasm)

46
Q
  • fine chromatin
  • auer rods
  • large cells
A

AML

47
Q
  • coarse chromatin
  • glycogen granules
  • smaller cells
A

ALL

48
Q

what is the first step in acute leukemia treatment

A

obtain complete remission:
- normal peripheral blood smear with resolution of cytopenias
- normal bone marrow with no excess blasts
- normal clinical status

49
Q

AML curative intent treatment

A

combo of anthracycline (daunorubicin or idarubicin) + cytarabine

50
Q

ALL treatment (philadelphia chromosome + and - )

A

philadelphia chromosome neg: Combination chemotherapy, including daunorubicin, vincristine, prednisone, and asparaginase

Philadelphia chromosome pos: tyrosine kinase inhibitor (dasatinib
or ponatinib) should be added to initial chemotherapy

51
Q

Proliferation of plasma cells (terminally differentiated B cells) that occurs most commonly in bone

Characterized by infiltration of the bone marrow, bone destruction, and paraprotein production*

Can cause bony destruction leading to:
* Hypercalcemia
* Bone pain
* Spinal cord compression
* Pathologic fractures

Malignant cells over-produce non-functional antibodies (proteins), resulting in immunodeficiency, elevated serum and urine protein (Bence Jones proteinuria)*

A

plasma cell myeloma

52
Q

how is a plasma cell myeloma diagnosis made?

A

analysis of serum protein electrophoresis and free light chains, and bone marrow biopsy

(light chains are abnormal)

53
Q

Older adults (median age 65 years)

MC presenting complaints are those related to anemia, bone pain, kidney disease, and infection

Bone pain –> back, hips, or ribs
May present as pathologic fracture, especially of femoral neck or vertebrae

Spinal cord compression from a plasmacytoma

Hyperviscosity syndrome –> mucosal bleeding, vertigo, nausea, visual disturbances, alterations
in mental status, hypoxia

Laboratory findings of elevated total protein, hypercalcemia, proteinuria, elevated ESR, abnormalities on serum protein electrophoresis obtained for symptoms or in routine studies

exam: pallor, bone tenderness, soft tissue masses

neurologic signs related to neuropathy or spinal cord compression

A

signs and symptoms of plasma cell myeloma

54
Q

what symptoms do you see in active myeloma (plasma cell myeloma)

A

CRAB symptoms
C- high calcium
R- renal (kidney problems)
A- anemia
B- bone problems

55
Q

Hallmark of plasma cell myeloma on lab findings

A
  • Anemia
  • rouleaux formation of RBC (grouped together in a line)
  • paraprotein on serum or urine protein electrophoresis (PEP) or
    immunofixation electrophoresis (IFE)
  • Positive Bence Jones Proteins: monoclonal light chains in urine
  • Bone marrow will be infiltrated by variable numbers of monoclonal plasma cell
56
Q

what do you see on plasma cell myeloma imaging (bone radiographs)

A

lytic lesions in axial skeleton (skull, spine, proximal long bones, and ribs)

Heme/Oncology (9 decks)

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