Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Heme/Oncology > hematologic malignancies > Flashcards

hematologic malignancies Flashcards

1
Q

blood cancer

A

myelodysplastic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A
  • hypercellular
  • erythroid hyperplasia
  • signs of abnormal erythopoeisis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

ringed sideroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

dwarf megakaryocytes with unilobed nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what defines MDS

A
  • genetic abnormalities
  • frequent cryogenic abnormalities involving chromosome 5 and 7
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how to differentiate between myelodysplasia and AML

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

low risk MDS treatment

A

improve blood clots
- erythropoietic growth factors

chromosomal abnormality
- lenalidomide

immunosuppressive therapy
- anti-thymocyte globulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

high risk MDS treatment

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Lymphocytic leukemias (ALL and CLL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Myeloproliferative disorder characterized by overproduction of myeloid cells

A

chronic myeloid leukemia (CML)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

translocation between long arms of chromosome 9 and 22

A

philadelphia chromosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Untreated CML can progress to an

A

“acute blast” phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
what do you see on bone marrow biopsy for CML (essential to confirm the phase of disease)
- karotype - bone marrow is hyper cellular, with left shifted myelopoiesis
25
when is blast phase CML diagnosed
when blasts comprise >20% of bone marrow cells
26
extreme hyperleukocytosis CML treatment
Emergent leukapheresis with myelosuppressive therapy
27
chronic phase CML treatment
tyrosine kinase inhibitor (imatinib)
28
advanced stage disease CML treatment
- tyrosine kinase inhibitor alone or in combo with myelosuppressive therapy - consider stem cell transplant
29
* 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
chronić lymphocytic leukemia (CLL)
30
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
signs and symptoms of CLL
31
what is the hallmark of CLL
isolated lymphocytosis
32
CLL bone marrow lab findings
small lymphocytes (diagnosis made from phenotype and genetic markers)
33
CLL smudge cells lab findings
cell remnants from fragile cells
34
early indolent CLL treatment
observation is standard of care
35
what are indication of starting therapy for CLL
- progressive fatigue - symptomatic lymphadenopathy - anemia - thrombocytopenia
36
CLL initial treatment
targeted biologic therapy: - BTK inhibitor as single agent (ibrutinib*, acalabrutinib, or zanubrutinib) - OR venetoclax* in combo with anti-CD20 antibody therapy (obinutuzumab)*
37
- chromosomal translocation - philadelphia chromosome - myeloid leukocytes (granulocytes and monocytes) - stop maturing and divide quickly - buildup and hepatosplenomegaly
CML
38
- chromosomal abnormalities - interfere with B cell receptors - lymphoid leukocytes (B cells) - stop maturing and die too slowly - buildup and lymphadenopathy
CLL
39
- 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
acute leukemia
40
median age 60 years (MC acute leukemia of adults)* Malignancy of myeloblasts
AML
41
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
ALL
42
- 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
signs and symptoms of acute leukemia
43
* 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
acute leukemia lab findings
44
hallmark of acute leukemia
pancytopenia with circulating blasts
45
characteristic of AML
auer rod (eosinophilic needle like inclusion in the cytoplasm)
46
- fine chromatin - auer rods - large cells
AML
47
- coarse chromatin - glycogen granules - smaller cells
ALL
48
what is the first step in acute leukemia treatment
obtain complete remission: - normal peripheral blood smear with resolution of cytopenias - normal bone marrow with no excess blasts - normal clinical status
49
AML curative intent treatment
combo of anthracycline (daunorubicin or idarubicin) + cytarabine
50
ALL treatment (philadelphia chromosome + and - )
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
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)*
plasma cell myeloma
52
how is a plasma cell myeloma diagnosis made?
analysis of serum protein electrophoresis and free light chains, and bone marrow biopsy (light chains are abnormal)
53
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
signs and symptoms of plasma cell myeloma
54
what symptoms do you see in active myeloma (plasma cell myeloma)
CRAB symptoms C- high calcium R- renal (kidney problems) A- anemia B- bone problems
55
Hallmark of plasma cell myeloma on lab findings
- 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
what do you see on plasma cell myeloma imaging (bone radiographs)
lytic lesions in axial skeleton (skull, spine, proximal long bones, and ribs)

Heme/Oncology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions