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Leukemias/Lymphomas Flashcards

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1
Q

Where do lymphomas originate?

A

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

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2
Q

Types of lymphoblastic neoplasms

A

acute lymphoblastic leukemias/lymphomas and chronic lymphoblastic leukemias/lymphomas

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3
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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4
Q

Most common form of childhood leukemia

A

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

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5
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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6
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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7
Q

Significance of MLL gene

A

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

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8
Q

2 basic categories of lymphomas

A

Hodgkin and Non-Hodgkin lymphoma

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9
Q

Characteristics of all leukemias

A

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

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10
Q

85% of acute lymphoblastic leukemias are…

A

B-cell leukemias

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11
Q

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

A

3-7 years

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12
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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13
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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14
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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15
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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16
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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17
Q

What is neurofibromatosis

A

mutation in tumor suppressor gene

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18
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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19
Q

Translocation in T-ALL

A

Between T-cell receptor chains and transcription factor genes

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20
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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21
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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22
Q

Clinical features in T-ALL

A

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

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23
Q

CLL and ALL more common in which age groups

A

CLL- elderly

All- 3-7 years

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24
Q

CLL diagnosis requires…

A

lymphocyte count HIGH >4,000/ul

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25
Most common leukemia of adults
CLL
26
CLL diagnosis
anemia, thrombocytopenia, high lymphocyte count >4,000/ul, HIGH WBC COUNT, lymphadenopathy, splenomegaly
27
WBC count in SLL vs. CLL
CLL- leukocytosis | SLL- leucopenia
28
Pheonotype of CLL
CD19, CD20, CD23, and CD5
29
What does a low level of surface expression of Ig in CLL tell you?
little ability for B cells to differentiate into plasma cells and produce antibodies, resulting in weak immune response
30
Translocations or deletions in CLL?
DELETIONS more common, especially in chromosomes 11, 13, and 17
31
Deletion in chromosome 13...
worse prognosis, because chromosome 13 contains the tumor suppressor gene
32
What would cause worse prognosis in CLL?
deletions of 11q and 17p, expression of ZAP-70, unmutated Ig
33
What contributes to increased susceptivility to infections in CLL?
Hypogammaglobulinemia- causes low levels of antibodies in the blood
34
What can CLL transform to?
Prolymphocyte transformation in 15-30% of patients, and transformation to diffuse large B-cell lymphoma (Richter syndrome) in 5-10% of patients
35
How to treat CLL?
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
36
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?
Acute myelogenous leukemia
37
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?
Acute lymphocytic leukemia from B-cell precursor
38
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
T-ALL
39
Patient presents with lymphadenopathy, splenomegaly on PE. CBC reveals increased lymphocyte count. Smear shows presence of smudge cells. Decreased humoral immunity, hypogammaglobulinemai
CLL
40
Tx for ALL, CLL
Chemo, BMT (For CLL, tx may not be necessary- splenectomy may be done to increase appetite and decrease pain)
41
Tx in AML
Induction treatment, cytarbine, anthracyclines (daunorubicin)
42
Daunorubicin
Anthracycline, DNA intercalater that prevents cells from going into mitosis given in AML tx
43
Cytarbine
S phase specific antimetabolite given in AML treatment
44
Prognosis of AML
50-60% reach complete remission, those that don't have drug resistance.
45
Post remission management of AML
stem cell transplant from peripheral blood
46
What is AML caused by?
associated with radiaction, chemo, chemicals
47
What most commonly causes CLL?
Deletions
48
What causes CML?
Philadelphia chromosome- 9:22 BCR-ABL translocation
49
Age group that CML affects?
45-55 years
50
Myelocyte bulge
More myelocytes than metamyelocytes present (if occurs in CML, means progression is rapid)
51
What cells are considered blasts in CML?
Myelocytes,myeloblasts, and promelanocytes
52
If you find blast cells in peripheral blood- is this normal or abnormal?
Blast cells not normally found in peripheral blood.
53
Types of blast cells
Immature precursor cells of either lymphocytes (lymphoBLASTS) or granulocytes (myeloBLASTS)
54
What is a promyelocyte
Intermediate between myeloblast and myelocyte
55
Neutrophil maturation
Myeloblast, promelanocyte, myelocyte, metamyelocyte, band, neutrophil
56
Tx for CML
SCL if very well matched donor. If not, GLeevac or Imatinib 400mg/day
57
Imatinib
blocks activity of tyrosine kinase, given in tx for CML (400mg/day)
58
Which leukemia would show a high number of neutrophils, basophils, and eosinophils?
Chronic myelogenous leukemia
59
Describe the triphasic course of CML
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
60
WHat is leukocyte alkaline phosphatase
enzyme important for phagocytosis by macrophages; test to rule out reactive leukocytosis
61
Levels of leukocyte alkaline phosphatase are low in what leukemia?
CML
62
What might CML progress to?
half progress to AML, about a third to ALL, and 10% to acute erythroleukemia
63
Is Chronic Neutrophilic Leukemia of lymphoid or myelogenous origin?
Myelogenous
64
Types of myeloproliferative disorders of myeloid type
CML, CNL, CEL
65
Types of myeloproliferative disorders of non-myeloid type
polycythemia vera, essential thrombocytopenia, and idiopathic mylofibrosis
66
What is CNL caused from?
t(15:19) translocation
67
What is CEL caused from?
translocation of PDGF alpha gene
68
What is PDGF
Tyrosine kinase activator, causes cell proliferation
69
What myeloproliferative disorders have JAK 2 mutation?
Polycythemia vera (90%), essential thrombocytopenia (30%), and idiopathic mylofibrosis (50%)
70
Diagnosis for PV
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
71
In deciding whether RBC mass is truly above normal-
if yes--true erythrocytosis. | If no- relative erythrocytosis
72
Tx for PV
Phlebotomy 1 unit removed/week 500ml. repeat until Hct is less than 45% and myelosuppressive therapy
73
Forms of myelosuppressive therapy in PV
For massive splenomegaly, thrombocytosis, and hyperuricemia
74
Tx for massive splenomegaly in PV
hydroxyurea or interferon
75
Tx for thrombocytosis in PV
Hydroxyura and anagrelide phosphodiesterase III inhibitor- inhibits megakaryocyte maturation to slow growth of platelets in bone marrow
76
Hyperuricemia definition and how to treat this in PV
high levels of uric acid in blood, treat with allopurinol
77
allopurinol
Tx for hyperuricemia (decreases effects of uric acid)
78
Why does PV have to be monitored carefullY/
can progress to AML in 5% of people
79
Why does Idiopathic myelofibrosis have to be monitored carefully?
can progress to acute leukemia in 10% of people
80
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?
most likely idipathic myelofibrosis. Tx with splenectomy if severe thrombocytopenia or cachexia, and allopurinol for tx of uric acid
81
Essential thrombocytosis should be monitored carefully because
5-10% can progress to AML
82
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.
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
83
Amicar
Medicine given to inhibit fibrinolysis
84
Tx of multiple myeloma
chemo- VAD vincristine, adriamycin, and dexamethasone
85
Characteristic signs of multiple myeloma
Bence jones proteins, rouleaux "roll of coins" appearance, russel bodies, dutcher bodies, lytic bone lesions, light-chain cast nephropathy, bone pain and fractures
86
pathogenesis of multiple myeloma
genetic predisposition, chronic antigenic stimulation, chromosomal abnormalities (high risk if not controlled by treatment)
87
what causes the rouleaux appearance of RBC's?
Large amounts of IgG non-specific antibodies

HEMATOLOGY (5 decks)

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