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From Flashcardlet > Leukemia/Lymphoma > Flashcards

Leukemia/Lymphoma Flashcards

1
Q

Where do leukemias originate?

A

Blood-producing tissue- the bone marrow

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2
Q

Where do lymphomas originate?

A

Cells of the immune tissue- secondary lymphatic structures like the spleen, liver, and lymph nodes

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3
Q

Reed-Sternberg cells

A

Histological characteristic of Hodgkin lymphoma

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4
Q

Do acute or chronic leukemias respond better to chemotherapy?

A

Acute leukemias respond better to chemotherapy

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5
Q

What is the genetic mutation behind CML?

A

Philadelphia chromosome t(9,22)

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6
Q

Are most ALL cases B- or T-cell in origin?

A

85% are B-cell leukemias

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7
Q

Why does pancytopenia occur in ALL?

A

The blast cells physically crowd out other cells

Blast cells release factors to suppress production of other cells

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8
Q

What is the nucleus/cytoplasm ratio like in ALL?

A

High N/C ratio, the nucleus is huge compared to the cytoplasm

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9
Q

Where can you find cells of a precursor B/T-cell leukemia?

A

Bone marrow

Peripheral blood

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10
Q

Where can you find cells of a precursor B/T-cell lymphoma?

A

Extramedullary tissues (nodes)

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11
Q

What population is most affected by B-cell ALL?

A

75% are <6 y.o.

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12
Q

TdT

A

Terminal deoxynucleotidyl transferase

A membrane marker to determine the maturation of a B-cell ALL

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13
Q

How likely is complete remission from precursor B-cell ALL for children?

A

> 90% achieve complete remission

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14
Q

What would a translocation in the MLL gene at 11q23 indicate?

A

Poor prognosis regardless of age

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15
Q

What causes bone pain in people (esp. children) with precursor B-cell ALL?

A

The leukemia can spread to the meninges and the periosteum

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16
Q

Is precursor B- or T-cell ALL more likely to have lymphomatous presentation with mediastinal adenopathy?

A

Precursor T-cell ALL

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17
Q

Where are the translocations in precursor T-cell ALL?

A

T-cell receptor chains

Transcription factor chains

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18
Q

What antigens do early T-cells display?

A

CD-7
CD-2
CD-5

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19
Q

What antigens do T-cells display after thymus maturation?

A

CD-1a
CD-3
CD-4
CD-8

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20
Q

What is the most common leukemia in adults?

A

Chronic Lymphocytic Leukemia

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21
Q

What level of WBCs is diagnostic for CLL?

A

> 4,000

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22
Q

What are some histologic characteristics of CLL?

A

An infiltrate of small WBCs
Smudge cells
Low expression of IgG

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23
Q

What surface antigens are present in CLL?

A

CD19
CD20
CD23
CD5

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24
Q

What type of genetic mutations are found in CLL?

A

Mostly deletions, translocations are rare

Deletions of 13, 11, 17

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25
Q

Which deletions in CLL have the worst prognosis?

A

Deletion of 13 because it carries tumor-suppressor genes
11q
17p

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26
Q

What is the difference in WBC count between CLL and SLL?

A

CLL has very high WBC counts (>200,000)

SLL has leukopenia (WBCs from nodes stop marrow production)

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27
Q

Explain how hemolytic anemia or thrombocytopenia can occur with CLL.

A

The functional B-cells produce auto-antibodies that destroy self cells (RBCs and platelets) in 10-15% of CLL patients

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28
Q

ZAP-70

A

A protein that augments signals produced by Ig receptor, means a worse CLL outcome

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29
Q

What percentage of CLL patients experience prolymphocytic transformation?

A

15-30%

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30
Q

Richter syndrome

A

Transformation to diffuse large B-cell lymphoma in 5-10% of CLL patients

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31
Q

Why is a splenectomy recommended for some CLL patients?

A

Removing an enlarged spleen can help them regain their appetite and decrease pain

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32
Q

What age group is most affected by acute myelogenous leukemia?

A

15 y.o. - adulthood

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33
Q

What kind of drugs have a strong association with AML?

A

Radiation
Alkylating agents
Benzenes

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34
Q

Auer rods

A

A histological characteristic of bone marrow with AML

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35
Q

Idiopathic mylofibrosis

A

Excess proliferation of fibrotic tissue in the marrow decreases production of blood cells

36
Q

What lab findings would indicate AML?

A

WBC count ~15,000
Auer rods
Dec reticulocytes
Normocytic normochromic anemia

37
Q

Cytarabine

A

S-phase specific antimetabolite

38
Q

Anthracyclines (daunorubicin)

A

DNA intercalater incorporates into the DNA, non-specific

39
Q

What is the prognosis for someone with AML?

A

60-75% achieve complete remission

40
Q

How would you manage a patient with AML after remission?

A

Stem cell transplant because relapses are common

41
Q

What is the common genetic basis for the myeloproliferative disorders?

A

They all have to do with tyrosine kinase

42
Q

What is the mutation associated with CML?

A

t(9,22) BCR-ABL translocation activates tyrosine kinase

43
Q

What is the mutation associated with CEL?

A

Translocation of PDGF alpha gene

PDGF is a tyrosine kinase activator

44
Q

JAK2

A

Tyrosine kinase mutation that causes prolonged life, not destroyed when it should be

45
Q

How does age affect the incidence of CML?

A

Incidence increases with age, but the median age range at presentation is 45-55

46
Q

Allopurinol

A

Treats elevated uric acid d/t increased cell death

47
Q

Why would someone with CML have sternal pain?

A

The marrow is compressed with increased myeloid cells in the nodes
Increased WBCs congregate in the nodes

48
Q

Why would someone with CML develop gout?

A

The increased WBCs cause increased cell death and breakdown of DNA, increasing the amount of uric acid

49
Q

Describe the myeloblast counts associated with the triphasic progression of CML.

A

Chronic: 20,000

50
Q

What is the life expectancy of someone with CML?

A

3-5 years after diagnosis

18 months after the accelerated phase

51
Q

Myelocyte bulge

A

More myelocytes than metamyelocytes because maturation can’t keep up with the increased production

52
Q

Reactive leukocytosis

A

Elevated WBC count for a good reason, need them to fight infection

53
Q

Leukocyte alkaline phosphatase

A

Enzyme necessary for WBCs to phagocytize, very low in CML so patients have hard time fighting infection even though WBCs are so high

54
Q

What % of a WBC differential should be neutrophils?

A

60-65%

55
Q

What % of a WBC differential should be basophils?

A

1-2%

56
Q

What % of a WBC differential should be eosinophils?

A

1-2%

57
Q

What % of a WBC differential should be lymphocytes?

A

25-35%

58
Q

What absolute WBC differential values would indicate CML?

A 
Absolute basophilia (in 100%)
Absolute eosinophilia (in 90%)
59
Q

How would you treat CML?

A

Young with good matched donor: allograft
Start Gleevac/Imatinib
If good response, maintain indefinitely
If bad response, consider allograft

60
Q

Imatinib

A

Gleevac

61
Q

What is the prognosis for polycythemia vera?

A

> 10 years with treatment, usually die of thrombosis or transformation to acute leukemia
12 months without treatment

62
Q

What are the causes of primary and secondary polycythemia vera?

A

Primary: bone marrow making too many RBCs
Secondary: hypoxia dependent (inc EPO) or hypoxia independent (tumor makes EPO)

63
Q

Spurious polycythemia

A

Relative erythrocytosis, a reduction in plasma volume

64
Q

What manifestation will you see in primary polycythemia vera that you won’t see in secondary?

A

Enlarged spleen (inc red pulp d/t inc RBCs)

65
Q

How does polycythemia vera affect blood pressure?

A

The increased RBCs increase volume, which increases BP

66
Q

Plethora

A

Cherry red cheeks

67
Q

How will absolute or relative erythrocytosis affect MCV?

A

Absolute: inc MCV
Relative: normal MCV

68
Q

What 2 clinical manifestations must be present to start thinking about diagnosing polycythemia vera?

A

Increased RBC mass

Normal O2 sat and EPO

69
Q

How would you treat polycythemia vera?

A

Phlebotomy to remove blood until Hct<45%

70
Q

Anagrelide

A

Phosphodiesterase III inhibitor, inhibits megakaryocyte maturation to dec platelets

71
Q

What percentage of people with polycythemia vera progress to an AML?

A

5% in 11-15 years

72
Q

Explain how a patient with essential thrombocytosis can acquire vWF disease.

A

The increased platelets bind to vWF and pull it out of solution, making the vWF unable to bind to subendothelial collagen

73
Q

Amicar

A

Inhibits fibrinolysis, used to treat essential thrombocytosis if patient is bleeding

74
Q

What is a histological characteristic of idiopathic myelofibrosis?

A

Teardrop/nucleated RBCs

75
Q

What are some systemic manifestations of idiopathic myelofibrosis?

A

Dry bone marrow tap
Osteosclerosis d/t fibrotic tissue
Splenic infarctions d/t fibrotic tissue
Gout

76
Q

How would you treat idiopathic myelofibrosis?

A

Splenectomy if cachexic or thrombocytopenia
Allopurinol
Supportive care

77
Q

What is the prognosis for someone with idiopathic myelofibrosis?

A

Median survival is 5 years
10% develop AML
50% of transplant patients have long-term survival

78
Q

What population is most at risk for developing multiple myeloma?

A

African American males

79
Q

What is multiple myeloma?

A

Tumor of B cells and plasma cells, likes to live in the bone tissue

80
Q

What are some of the theories behind the cause of multiple myeloma?

A

Chronic antigenic stimulation of B cells causes plasma cell malignancy
Chromosomal abnormalities

81
Q

Rouleaux

A

“Roll of coins” appearance of RBCs, Abs cause them to stick together in multiple myeloma

82
Q

Bence Jones proteins

A

Ig light chains present in the urine, diagnostic for multiple myeloma

83
Q

Russell bodies

A

Eosinophilic cytoplasmic inclusions of excess Ig

84
Q

Dutcher bodies

A

Eosinophilic nuclear inclusions of excess Ig

85
Q

“Punched out lesions”

A

Seen on x-ray d/t multiple myeloma

86
Q

How would you diagnose multiple myeloma?

A

X-ray to look for bone lesions
Biopsy to look for sheets of plasma cells in bone marrow
Significant monoclonal IgM-component in serum or urine

87
Q

How would you treat multiple myeloma?

A

Chemotherapy, VAD (2-3 year survival)

Only 6-12 month survival without chemo

From Flashcardlet (22 decks)

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