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Hem/Onc 2 > Clinical > Flashcards

Clinical Flashcards

1
Q

This is the early bone marrow hematopoietic cell.

A

Blast cell

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2
Q

What happend to bone marrow to cause acute leukemia?

A

Failure

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3
Q

What are the 3 markeres for AML?

A

CD13, CD33, MPO

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4
Q

Do mainly kids or adults get AML?

A

Adults

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5
Q

What 2 conditions can make u eligable for stem cell transplant for the treatment of AML?

A

< 65 y/o

HLA matching a sibling donor

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6
Q

What is the main detereminant for therapy for AML?

A

age

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7
Q

What is the regiment for AML therapy?

A

4 blocks, each about 1 wk

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8
Q

What is the treatment if a hemorrhagic syndrome develops in promyelocytic variant AML?

A

platelets with FFP

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9
Q

What drug can cause the prolfieration of N0 that follows differentiation of promyelocytes from the bone marrow?

A

ATRA

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10
Q

What is the treatment of ATRA syndrome?

A

Dexamethasone

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11
Q

What do u treat the elderly with in AML over 70?

A

supportive care with or without gentle single-drug chemo

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12
Q

What is the treatment options for relapsed AML?

A

Further chemo
stem cell transplant if tolerable and have a donor
arsenic trioxide for relapsed M3 variant

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13
Q

This is teh small # of leukemic cells that remain in the pt during treament, or during remission.

A

Minimal residual disease (MRD)

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14
Q

What can MRD do?

A

cause relpase in cancer and leukemia

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15
Q

Are chronic or acute leukemias harder to treat?

A

Chronic

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16
Q

What % of leukemias are CML?

A

15%

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17
Q

What is the gene mutation in CML?

A

t(9;22)

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18
Q

What age range is at risk for CML?

A

40-60

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19
Q

Which organ is enlarged in CML?

A

Spleen

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20
Q

What is the drug that is used to treat CML by blocking tyrosine kinase activity?

A

Imatinib (glivec)

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21
Q

What is the optimal response to imatinib?

A

complete cytogenic response

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22
Q

If the pt has a suboptimal response to imatinib in the Tx of CML, what other 2 drugs can u give?

A

Dasatinib

Nilotinib

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23
Q

What do Dasatinib and Nilotinib do to help Tx CML?

A

overcome resistance to imatinib or early allogenic stem cell transplant

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24
Q

What is the overall survival rate in CML pts in the Tx with imatinib?

A

89%

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25
Q

What does hydroxyurea do to help CML pts?

A

it can control and maintain the white cell count in chronic phase

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26
Q

How long do u have to take hydroxyurea in the Tx of CML?

A

Forever.

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27
Q

After the white cell count has been controlled by hydroxyurea, what has been used to keep the white cell count low?

A

a-interferon

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28
Q

Waht is the only established curative treatment for CML?

A

Allogenic stem cell transplant

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29
Q

What are the 2 reservations for the use of stem cell transplant for CML Tx?

A

if u fail with imatinib and are < 65 y/o

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30
Q

This is when there is 20% or more blasts in the marrow and may occur rapidly over days or weeks.

A

Acute transofrmation

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31
Q

What are the features of the accelerated phase?

A

anemia, thrombocytopenia and an increase in basophils, eosinophils or blast cells in the blood and marrow

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32
Q

What are the 3 main myeoloproliferative neoplasms (MPN)?

A

PV
Pimary myelofibrosis
ET

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33
Q

What mutation is common in all MPN’s?

A

JAK2 tyrosine kinase

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34
Q

What is the normal role of JAK2 tyrosine kinase?

A

acts as a signal transduction molecule for the EPO and TPO receptors.

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35
Q

This is the disease state in which the proportion of blood volume that is occupied by red blood cells increases.

A

Polycythemia

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36
Q

This is the form of polycythemia where an increased hct due to a decreased plasma volume and normal RBC mass.

A

Relative polycythemia

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37
Q

This is the form of polycythemia when the hct levels are greater than 18 g/dL in males and 16.5 g/dL in females.

A

Absolute polycythemia

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38
Q

This is a myeloproliferative disorder of RBC’s that results from activating mutations of JAK2 tyrosine kinase.

A

PV

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39
Q

What are the main clinical manifestations of PV?

A

postbathing pruritis, fatigue, erythromyelelgia (acral dyesthesias and ertythema), headache, dizziness, unexplained wt loss, joint symptoms, dyspnea, and epigastric distress.

40
Q

What are the main treatment options for PV?

A

Phelbotomy, low dose ASA, hydroxyurea, INFa, and radiophosphorus.

41
Q

This is a clonal hematologic disorder in which pts present with thrombocytosis and sometimes leukocytosis. It’s from the overproduction of platelets by megakryocytes in the bone marrow

42
Q

What are the clinical manifestations to ET?

A

bleeding and thrombosis (counterinuitive lol), erythromelalgia, possible splenomegaly

43
Q

What is teh treatment for low risk ET?

44
Q

What are the 2 ways u can treat high risk ET?

A 
Platelet apheresis (in emergencies)
Cytoreductive therapy (hydroxyurea, anagrelide, INFa)
45
Q

This is the condition where there is progressive reactive fibrosis (scarring) of the bone marrow occurs –> blood forms in sites other than the bone marrow (like liver or spleen) –> enlargement of liver/spleen

A

Primary myelofibrosis (PMF)

46
Q

What is the main organ problem seen on exam in PMF?

A

Massive splenomegaly

47
Q

What 2 things do u see on smear in PMF?

A

nucleated RBC’s and teardrop cells

48
Q

This is the presence of too many mast cells and CD34+ mast cell precursors in a person’s body.

A

Mastocytosis

49
Q

What mutation causes mastocytosis?

A

KIT tyrosine kinase

50
Q

What are the 2 clinical presentations of mastocytosis?

A

Skin lesions and allergic Sx

51
Q

What is the DOC for mastocytosis?

52
Q

What is the cause of priamry and secondary myelodysplasia?

A

primary- unknown

secondary- post cancer Tx

53
Q

Usually there arent Sx in myelodysplasia, but what are the Sx if there are any?

A

Infections or easy bruising/bleeding

54
Q

Who is at risk for ALL?

55
Q

What are the 3 manifestatiosn from bone marrow failure in ALL?

A

Anemia
Neutropenia
Thrombocytopenia

56
Q

What is the morphology of the RBC’s in ALL?

A

normochromic, normocytic anemia

57
Q

How many chromosomes characterizes hyperdiploid?

58
Q

Does hyperdiploid cells in ALL have a good or bad prognosis, when compared to hypodiploid?

59
Q

High dose systemic methotrexate given IV, intrathecal methotrexate or cytosine arabinoside or cranial irradiation are all used to treat what?

A

Cranial disease

60
Q

What is the maitenance therapy for ALL?

A

Daily oral mercaptopurine + once weekly oral methotrexate for 2 years

61
Q

In addition to oral therapy for ALL, what IV therapy is added monthly for ALL?

A

IV vincristine with a short course of oral corticosteroids

62
Q

What is the best treatment for ALL relapse?

A

Allogenic stem cell transplant

63
Q

What is it called when there is a condition that resembles CLL but does not meet criteria for CLL + does not require treatment?

64
Q

For the following indicators, what the results of them for a BAD prognosis in CLL?

Stage
Sex
Lymphocute doublign time
Bone marrow biospy appearance
Chromsomes
VH immunoglobulin gene
ZAP expression
CD38 expression
CLLU.1 expression
LDH
A 
Stage- Binet B, C
Sex- male
Lymphocute doublign time- rapid
Bone marrow biospy appearance- diffuse
Chromsomes- trisomy 12, del 17p, del 11q23
VH immunoglobulin gene- unmutated
ZAP expression- high
CD38 expression- +
CLLU.1 expression- high
LDH- raised
65
Q

Since cure rates in CLL are rare, what is the approach to therapy?

A

Conservative, aiming for Sx control

66
Q

When is chlorambucil given in CLL to induce remission?

A

given for several months

67
Q

The use of Rituximab and other monoclonal AB’s in CLL is used for what?

A

used in resistant and relapsed disease

68
Q

What is teh indication for the use of corticosteroidds in CLL?

A

bone marrow failure

69
Q

This is the conditon which is like CLL but there is a majority of prolymphocytes in the blood (big suckers) and they have a nucleolus.

70
Q

What are the 2 drugs for Hairy cell leukemia?

A

2-chlorodeoxyadenosine

Deoxycoformycin

71
Q

What do the lymphocytes look like in LGL-L?

A

abundant cytoplasm and large azurophilic granules

72
Q

Which 2 WBC’s are transformed in LGL-L?

73
Q

What age do u get LGL-L?

74
Q

What is the clinical presentation of LGL-L?

A

cytopenia, esp neutropenia

75
Q

What happens to the ESR and CRP in HL?

A

They’re raised

76
Q

What is characterized by stage I HL?

A

node involvement in one lymph node area

77
Q

What is characterized by stage II HL?

A

disease involving two or more lymph nodal areas confined to one side of the diaphragm

78
Q

What is characterized by stage III HL?

A

disease involving lymph nodes above and below the diaphragm

79
Q

What is characterized by stage IV HL?

A

involvement outside the lymph node areas and refers to diffuse or disseminated disease in the bone marrow, liver and other extranodal sites.

80
Q

What should men do before Tx to HL?

A

freeze their sperm

81
Q

What is the treatment for stage 1 and 2A of HL?

A

radiotherapy alone

82
Q

What is the treatment for stage 3 and 4 of HL?

83
Q

What is the combo chemo regimen for HL?

A

Adriamycin, bleomycin, vinblastine and dacarbazine (ABVD) is given in 6 cycles (or 4 following complete remission)

84
Q

What is the cure rate for each stage of HL?

A

I- 90%
II- 90%
III- 80%
IV- 65%

85
Q

Which form of NHL (low or high grade) is easier to cure and often curable?

A

High grade

the worse the better?

86
Q

This is the term for the presence of a monoclonal immunoglobulin band in the serum

A

Paraproteinemia

87
Q

What type of MM is when there’s plasma cells in the bone marrow (plasma cell count is >10%) but there is no evidence of tissue damage?

A

Asymptomatic (smouldering) MM

88
Q

What does the CRAB acronym stand for in the Dx of MM?

A

hyperCalcemia
Renal impairment
Anemia
Bone disease

89
Q

What is the Tx for MM in pts that are 65-70 and need intensive therapy?

A

severeal corses of chemo, allogenic stem cell trasnplant

90
Q

What is the non-intensive therapy for 70+ pts with MM?

A

monthly oral alkylating gane MELPHALIN

91
Q

What drug is the 1st line therapy and management of relapsed disease in MM?

A

Thalidomide

92
Q

When is Bortezomib used in the Tx of MM?

A

Refractory dz

93
Q

What are pts with MGUS at risk for later in life?

A

Myeloma or lymphoma

94
Q

What is the stain used to identify amyloidosis?

A

Congo red stain

95
Q

What do u see under polarized light after staining with Congo red for amyloidosis?

A

Red-green birefringence

Apple-green

96
Q

What is the msot common cause of polycythemia?

A

Hyperviscosity syndrome

97
Q

What pts are at risk for hyperviscosity syndrome?

A

myeloma, Waldenstrom’s macroglobulinemia, CML, or acute leukemias

Hem/Onc 2 (5 decks)

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