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From Flashcardlet > Heme Deck 5 > Flashcards

Heme Deck 5 Flashcards

2
Q

Where do lymphomas originate?

A

Secondary lymphatic structures-begin in cells of the immune system (lymph nodes, spleen)

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3
Q

Types of lymphoblastic neoplasms

A

acute lymphoblastic leukemias/lymphomas and chronic lymphoblastic leukemias/lymphomas

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4
Q

How are acute lymphoblastic leukemias/lymphomas classified?

A

Precursor is either B-cell or T-cell lymphoblastic leukemia or lymphoma

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5
Q

Most common form of childhood leukemia

A

B-ALL. Acute lymphoblastic leukemia arising from precursor B-cell lymphoblastic leukemia

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6
Q

How to diagnose B-cell ALL (leukemia)?

A

Bone marrow smear- fine chromatin pattern, high N/C ratio, 1-2 prominent nucleoli

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7
Q

Prognosis of child precursor B-cell ALL (leukemia?)

A

Complete remission in more than 90%, but translocations involving the MLL gene at 11q23 have poor prognosis

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8
Q

Significance of MLL gene

A

Translocations in this gene at 11q23 in B-cell ALL (leukemia) have poor prognosis

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9
Q

2 basic categories of lymphomas

A

Hodgkin and Non-Hodgkin lymphoma

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10
Q

Characteristics of all leukemias

A

Anemia (fatigue), thrombocytopenia (bleeding), and low white cell count (infections)

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11
Q

85% of acute lymphoblastic leukemias are…

A

B-cell leukemias

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12
Q

What age would you suspect of a patient diagnosed with acute lymphoblastic leukemia/lymphoma?

A

3-7 years

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13
Q

4 year old child presents with easy brusing, bleeding, fatigue, and constant infections. You order CBC and find low platelet count, low WBC’s, low RBC’s (anemia). B cells elevated. Upon PE, you feel enlarged liver, spleen. Child also has bone pain and anorexia. Dx and tx?

A

B-ALL. Tx- chemo, then BMT

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14
Q

What is TDT

A

equals DNTT (terminal transferase)- expressed in IMMATURE, pre-B, or pre-T lymphoid cells and acute lymphoblastic leukemia/lymphoma cells. This is important marker that tells you about level of maturation in leukemia

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15
Q

What can markers on the cells tell you?

A

Tell you about lineage (B cell vs. T cell) and level of maturation

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16
Q

What markers tell you if leukemia is precursor of lymphoid cell vs. more differentiated cell (mature B or T cell?)

A

TdT, CD34, and CD10

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17
Q

How does B-ALL occur?

A

Theory- due to translocations. Environment and genetics also may predispose a person- radiation, organic solvents, NF (neurofibromatosis), and down syndrome

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18
Q

What is neurofibromatosis

A

mutation in tumor suppressor gene

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19
Q

Prevalence of T-ALL in children and adults

A

T-ALL accounts for 15% of all childhood ALL, 25% of all ALL in adults is T-ALL

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20
Q

Translocation in T-ALL

A

Between T-cell receptor chains and transcription factor genes

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21
Q

Pathology of T-ALL

A

Presence of early T-cell antigens- CD7 followed by CD2 and CD5. During thymic differentiation the T-cells become positive for CD1a and CD3, CD4 and CD8. Lymphoblasts are positive for the TdT enzyme.

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22
Q

Prognosis of T-ALL

A

worse in children compared to B-ALL, but better in adults compared to B-ALL

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23
Q

Clinical features in T-ALL

A

anemia, thrombocytopenia, WBC count HIGH, mediastinal masses, lymphadenopathy, organomegaly, pleural effusions present

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24
Q

CLL and ALL more common in which age groups

A

CLL- elderly All- 3-7 years

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25
Q

CLL diagnosis requires…

A

lymphocyte count HIGH >4,000/ul

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26
Q

Most common leukemia of adults

A

CLL

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27
Q

CLL diagnosis

A

anemia, thrombocytopenia, high lymphocyte count >4,000/ul, HIGH WBC COUNT, lymphadenopathy, splenomegaly

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28
Q

WBC count in SLL vs. CLL

A

CLL- leukocytosisSLL- leucopenia

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29
Q

Pheonotype of CLL

A

CD19, CD20, CD23, and CD5

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30
Q

What does a low level of surface expression of Ig in CLL tell you?

A

little ability for B cells to differentiate into plasma cells and produce antibodies, resulting in weak immune response

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31
Q

Translocations or deletions in CLL?

A

DELETIONS more common, especially in chromosomes 11, 13, and 17

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32
Q

Deletion in chromosome 13…

A

worse prognosis, because chromosome 13 contains the tumor suppressor gene

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33
Q

What would cause worse prognosis in CLL?

A

deletions of 11q and 17p, expression of ZAP-70, unmutated Ig

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34
Q

What contributes to increased susceptivility to infections in CLL?

A

Hypogammaglobulinemia- causes low levels of antibodies in the blood

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35
Q

What can CLL transform to?

A

Prolymphocyte transformation in 15-30% of patients, and transformation to diffuse large B-cell lymphoma (Richter syndrome) in 5-10% of patients

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36
Q

How to treat CLL?

A

Tx may not be necessary depending on cytogenetics. Otherwise, can do chemo, BMT. Splenectomy is option- will relive pain and allow patient to eat more. But complications

37
Q

Patient presents with classic symptoms of leukemia and you have to decide which one it is. Hepatomegaly, splenomegaly, and anorexia found on PE. CBC reveals leukocytosis AND leukopenia. anemia is present, but there are decreased reticulocytes. Smear shows presence of Auer rods. Diagnosis?

A

Acute myelogenous leukemia

38
Q

Patient presents with classic symptoms of leukemia and you are trying to figure out what type it is. Hepatomegaly, splenomegaly, and anorexia upon PE seen. Patient complaining of bone pain. Smear shows fine chromatin pattern of lymphocytes, high N/C ratio, and 1-2 large nucleoli. Markers for CD19, TdT, CD34, and CD10 present. DIagnosis?

A

Acute lymphocytic leukemia from B-cell precursor

39
Q

Which leukemia is this- patient presents with leukocytosis, pleural effusions due to mediastinal masses and lymphadenopathy. Markers show Tdt, CD 7 followed by CD 2 and CD5, and CD1a and CD3, CD4, CD8

A

T-ALL

40
Q

Patient presents with lymphadenopathy, splenomegaly on PE. CBC reveals increased lymphocyte count. Smear shows presence of smudge cells. Decreased humoral immunity, hypogammaglobulinemai

A

CLL

41
Q

Tx for ALL, CLL

A

Chemo, BMT (For CLL, tx may not be necessary- splenectomy may be done to increase appetite and decrease pain)

42
Q

Tx in AML

A

Induction treatment, cytarbine, anthracyclines (daunorubicin)

43
Q

Daunorubicin

A

Anthracycline, DNA intercalater that prevents cells from going into mitosis given in AML tx

44
Q

Cytarbine

A

S phase specific antimetabolite given in AML treatment

45
Q

Prognosis of AML

A

50-60% reach complete remission, those that don’t have drug resistance.

46
Q

Post remission management of AML

A

stem cell transplant from peripheral blood

47
Q

What is AML caused by?

A

associated with radiaction, chemo, chemicals

48
Q

What most commonly causes CLL?

A

Deletions

49
Q

What causes CML?

A

Philadelphia chromosome- 9:22 BCR-ABL translocation

50
Q

Age group that CML affects?

A

45-55 years

51
Q

Myelocyte bulge

A

More myelocytes than metamyelocytes present (if occurs in CML, means progression is rapid)

52
Q

What cells are considered blasts in CML?

A

Myelocytes,myeloblasts, and promelanocytes

53
Q

If you find blast cells in peripheral blood- is this normal or abnormal?

A

Blast cells not normally found in peripheral blood.

54
Q

Types of blast cells

A

Immature precursor cells of either lymphocytes (lymphoBLASTS) or granulocytes (myeloBLASTS)

55
Q

What is a promyelocyte

A

Intermediate between myeloblast and myelocyte

56
Q

Neutrophil maturation

A

Myeloblast, promelanocyte, myelocyte, metamyelocyte, band, neutrophil

57
Q

Tx for CML

A

SCL if very well matched donor. If not, GLeevac or Imatinib 400mg/day

58
Q

Imatinib

A

blocks activity of tyrosine kinase, given in tx for CML (400mg/day)

59
Q

Which leukemia would show a high number of neutrophils, basophils, and eosinophils?

A

Chronic myelogenous leukemia

60
Q

Describe the triphasic course of CML

A

CHronic phase- less than 10% myeloblasts in blood or bone marrow, accelerated phase has 10-19% myeloblasts, and blast crisis- more than 20% myeloblasts. Can be biphasic if skips accelerated phase- very difficult to treat in these cases

61
Q

WHat is leukocyte alkaline phosphatase

A

enzyme important for phagocytosis by macrophages; test to rule out reactive leukocytosis

62
Q

Levels of leukocyte alkaline phosphatase are low in what leukemia?

A

CML

63
Q

What might CML progress to?

A

half progress to AML, about a third to ALL, and 10% to acute erythroleukemia

64
Q

Is Chronic Neutrophilic Leukemia of lymphoid or myelogenous origin?

A

Myelogenous

65
Q

Types of myeloproliferative disorders of myeloid type

A

CML, CNL, CEL

66
Q

Types of myeloproliferative disorders of non-myeloid type

A

polycythemia vera, essential thrombocytopenia, and idiopathic mylofibrosis

67
Q

What is CNL caused from?

A

t(15:19) translocation

68
Q

What is CEL caused from?

A

translocation of PDGF alpha gene

69
Q

What is PDGF

A

Tyrosine kinase activator, causes cell proliferation

70
Q

What myeloproliferative disorders have JAK 2 mutation?

A

Polycythemia vera (90%), essential thrombocytopenia (30%), and idiopathic mylofibrosis (50%)

71
Q

Diagnosis for PV

A

Raised red cell mass (females Hb more than 16.5, male HB more than 18.5) and Normal Oxygen saturation and normal or low EPO level PLUS 1 A or 2 B

72
Q

In deciding whether RBC mass is truly above normal-

A

if yes–true erythrocytosis.If no- relative erythrocytosis

73
Q

Tx for PV

A

Phlebotomy 1 unit removed/week 500ml. repeat until Hct is less than 45% and myelosuppressive therapy

74
Q

Forms of myelosuppressive therapy in PV

A

For massive splenomegaly, thrombocytosis, and hyperuricemia

75
Q

Tx for massive splenomegaly in PV

A

hydroxyurea or interferon

76
Q

Tx for thrombocytosis in PV

A

Hydroxyura and anagrelide phosphodiesterase III inhibitor- inhibits megakaryocyte maturation to slow growth of platelets in bone marrow

77
Q

Hyperuricemia definition and how to treat this in PV

A

high levels of uric acid in blood, treat with allopurinol

78
Q

allopurinol

A

Tx for hyperuricemia (decreases effects of uric acid)

79
Q

Why does PV have to be monitored carefullY/

A

can progress to AML in 5% of people

80
Q

Why does Idiopathic myelofibrosis have to be monitored carefully?

A

can progress to acute leukemia in 10% of people

81
Q

Patient with splenomegaly, marrow fibrosis leading to thrombocytopenia, mild anemia, teardrop, nucleated RBC’s, dry marrow tap due to fibrosis probably, gout, hypersegmented neutrophils. Diagnosis and tx?

A

most likely idipathic myelofibrosis. Tx with splenectomy if severe thrombocytopenia or cachexia, and allopurinol for tx of uric acid

82
Q

Essential thrombocytosis should be monitored carefully because

A

5-10% can progress to AML

83
Q

Patient presents with splenomegaly, bleeding, easy bruising. CBC reveals platelet count over 500,000/ul, normal RBC. Prolonged bleeding time, absent philadelphia chromosome. Diagnosis and Tx? Cause is unknown.

A

Essential thrombocytosis- if asymptomatic and less than 60 years, no tx. If more than 60 and neuro sx present, give hydroxyurea or angrelide. To decrease bleeding (because using up all platelets in clots), give amicar

84
Q

Amicar

A

Medicine given to inhibit fibrinolysis

85
Q

Tx of multiple myeloma

A

chemo- VAD vincristine, adriamycin, and dexamethasone

86
Q

Characteristic signs of multiple myeloma

A

Bence jones proteins, rouleaux “roll of coins” appearance, russel bodies, dutcher bodies, lytic bone lesions, light-chain cast nephropathy, bone pain and fractures

87
Q

pathogenesis of multiple myeloma

A

genetic predisposition, chronic antigenic stimulation, chromosomal abnormalities (high risk if not controlled by treatment)

88
Q

what causes the rouleaux appearance of RBC’s?

A

Large amounts of IgG non-specific antibodies

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