Brainscape's Knowledge GenomeTM

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


See full index

STEP > Heme Onc Part III > Flashcards

Heme Onc Part III Flashcards

1
Q

Auer rods seen mostly in

A

APL (formerly M3 AML)

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

Other impt finding in AML

A

Increased myeloblasts on peripheral smear

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

APL subtype translocation

A

t(15;17)

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

effect of all-trans retinoid acid?

A

Induces differentiation of promyelocytes.

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

RF’s for AML

A

1) alkylating therapy
2) radiation
3) myeloproliferative disorders
4) Down syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

median age at diagnosis in CML

A

64

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Blast crisis

A

CML acceleration and transformation to AML or ALL.

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

How do you distinguish CML from leukemoid reaction?

A

Very low LAP in CML (low activity in malignant neutrophils) vs benign neutrophilic with leukemia in which LAP is increased.

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

Burkitt’s translocation

A

8,14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens with chromosome 14 translocations?

A

The Ig heavy chain genes on chromosome 14 are normally constitutively expressed. When other genes (c-myc or BCL-2) translocate next to this gene, they become over expressed.

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

ALL translocation can rarely be…

A

9;22, BCR-ABL/philadelphia chromosome

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

Mantle cell activation

A

Cyclin D1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

mantle cell translocation

A

11,14

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

Folicular lymphoma translocation

A

14,18

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

APL translocation

A

15,17

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

Langerhans presentation

A

lytic bone lesions in a child + skin rash or recurrent otitis media with a mass involving the mastoid bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cell markers in langerhans

A

S-100 or CD1a

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

Chronic myeloproliferative disorder gene association

A

V617F JAK2 mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

myeloproliferative disorders…

A

1) polycythemia vera
2) ET
3) myelofibrosis
4) CML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Causes of relative polycythemia

A

1) dehydration

2) burns

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

Relative polycythemia

1) plasma volume
2) RBC mass
3) O2 sat
4) EPO levels

A

1) decreased
2) no difference
3) no difference
4) no difference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Appropriate absolute

1) plasma volume
2) RBC mass
3) O2 sat
4) EPO levels

A

1) no difference
2) increased
3) decreased
4) increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Causes of appropriate absolute polycythemia

A

1) lung disease
2) congenital heart disease
3) high altitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

INAppropriate absolute

1) plasma volume
2) RBC mass
3) O2 sat
4) EPO levels

A

1) no change
2) increased
3) no change
4) increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Causes of inappropriate absolute

A

Due to ectopic EPO secretion

1) malignancy (eg, RCC, HCC)
2) hydronephrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Polycythemia vera

1) plasma volume
2) RBC mass
3) O2 sat
4) EPO levels

A

1) Increased
2) Very increased
3) No difference
4) Decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

polycythemia vera etiology

A

Decreased EPO production due to negative feedback suppressing renal EPO production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

heparin mechanism

A

Lowers activity of thrombin and factor Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what do you need to monitor with heparin?

A

PTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

heparin AE’s

A

Bleeding + thrombocytopenia + osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Differences between LMWH and heparin

A

LMWH’s act more on factor Xa + have better bioavailability + 2-4 times longer half-life.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

HIT etiology

A

IgG antibodies against heparin-bound platelet factor 4 (PF4). Antibody-heparin-PF4 complex activates platelets leading to thrombosis and thrombocytopenia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

direct thrombin inhibitors

A

bivalirudin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

bivalirudin uses

A

1) venous thromboembolism

2) afib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

bivaluridin AE’s

A

Bleeding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How do you treat bleeding associated with bivalirudin?

A

Can try activated prothrombin complex concentrates (PCC) and/or fibrinolytic (eg, tranexamic acid).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Cause of gynecomastia in cirrhosis?

A

Failure of the liver to degrade estrogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is warfarin metabolism affected by?

A

Polymorphisms in the gene for vitamin K epoxide reductase complex (VKORC1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What do you need to monitor with warfarin?

A

PT + INR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Warfarin half-life

A

Long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

warfarin pharmacokinetic point

A

Proteins C and S have shorter half-lives than clotting factors II, VII, IX, and X, resulting in early transient hyper coagulability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

heparin structure

A

Large, anionic, acidic polymer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

warfarin structure

A

small, amphipathic molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Heparin site of action

A

blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

warfarin site of action

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

heparin mechanism

A

activates antithrombin, which decreases the action of IIa (thrombin) and factor Xa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Would heparin or warfarin inhibit coagulation in vitro?

A

heparin, but not warfarin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

PE prophylaxis drug

A

rivaroxaban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Stroke prophylaxis in patients with Afib?

A

Apixaban, rivaroxaban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

direct factor Xa inhibitors

A

Apixaban, rivaroxaban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

thrombolytics

A

Alteplase (tPA)
reteplase (rPA)
*streptokinase
tenecteplase (TNK-tPA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

thrombolytics labs

A

Increased PT + increased PTT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

thrombolytics contraindications

A

1) bleeding
2) history of intracranial bleeding
3) recent surgery
4) known bleeding diathesis
5) severe HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

thrombolytics bleeding managment

A

aminocaproic acid. Can also use fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the ADP receptor inhibitors?

A

clopidogrel
prasugrel
ticagrelor (reversible)
ticlopidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

ADP receptor inhibitor mechanism

A

1) inhibit platelet aggregation by irreversibly blocking ADP receptors
2) *prevent expression of glycoproteins IIb/IIIa on platelet surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Drug used for coronary stunting?

A

ADP receptor inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

other uses for ADP receptor inhibitors?

A

1) ACS

2) decrease incidence or recurrence of thrombotic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

ticlopidine AE

A

neutropenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Other AE possible with ADP receptor inhibitors?

A

TTP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

PDE-III inhibitors?

A

Cilostazol

Diypridamole

62
Q

PDE-III mechanism?

A

Increases cAMP in platelets, resulting in inhibition of platelet aggregation. Vasodilators

63
Q

What do you use for angina prophylaxis?

A

cilostazol, dipyridamole

64
Q

Other uses for PDE-III inhibitors?

A

1) claudication
2) coronary vasodilation
3) prevention of stroke or TIAs

65
Q

PDE-III inhibitors AEs

A

Nausea + headache + facial flushing + hypotension + abdominal pain.

66
Q

GP IIb/IIIa inhibitors?

A

abciximab, eptifibatide, tirofiban

67
Q

GP IIb/IIIa inhibitor MOA?

A

Prevent aggregation.

68
Q

Abciximab composition

A

monoclonal antibody Fab fragments

69
Q

GP IIb/IIIa use..

A

1) unstable angina

2) percutaneous transluminal coronary angioplasty

70
Q

GP IIb/IIIa AE’s

A

bleeding + thrombocytopenia

71
Q

cell cycle-independent cancer drugs?

A

1) Platinum agents

2) alkylating agents

72
Q

hydroxyurea MOA

A

Inhibits ribonucleotide reductase

73
Q

cisplatin MOA?

A

cross-links DNA

74
Q

how do alkylating agents work?

A

cross-link DNA

75
Q

Bleomycin MOA

A

Induces free radical formation –> DNA strand breakage

76
Q

Dactinomycin, doxorubicin MOA

A

intercalators

77
Q

etoposide MOA

A

inhibits topoisomerase *II

78
Q

irinotecan MOA

A

inhibits topoisomerase *I

79
Q

vinca alkaloid mechanism

A

inhibit microtubule formation

80
Q

What activates azathioprine, 6-MP?

A

HGPRT

81
Q

azathioprine relationship to 6-MP

A

Azathioprine is metabolized into 6-MP.

82
Q

What do you use to wean patients off steroids in chronic disease?

A

Azathioprine, 6-MP

83
Q

Other use for azathioprine, 6-MP

A

steroid-refractory chronic disease

84
Q

azathioprine, 6-MP AE’s

A

myelosuppresion, GI, liver

85
Q

cladribine MOA

A

purine analog –> multiple mechanisms (inhibition of DNA polymerase, DNA strand breaks)

86
Q

cladribine AE’s

A

myelosuppression + nephrotoxicity + neurotoxicity

87
Q

Cytarabine MOA

A

pyrimidine analog –> inhibition of DNA polymerase

88
Q

cytarabine also known as…

A

arabinofuranosyl cytidine

89
Q

Cytarabine AE’s

A

myelosuppression with megaloblastic anemia. pancytopenia.

90
Q

5-FU MOA

A

pyrimidine analog bioactivated to 5-FdUMP, which covalently complexes folic acid –> inhibition of thymidylate synthase –> decreased dTMP –> decreased DNA synthesis.

91
Q

5-FU uses

A

1) colon cancer
2) pancreatic cancer
3) basal cell carcinoma (topical)

92
Q

5-FU commonly combined with…

A

leucovorin (enhances effects but also worsens myelosuppression)

93
Q

methotrexate mechanism

A

Folic acid analog that competitively inhibits dihydrofolate reductase leading to decreased dTMP and decreased DNA synthesis

94
Q

cancers methotrexate is used for

A

1) ALL
2) lymphomas
3) choriocarcinoma
40 Sarcomas

95
Q

How do you prevent myelosuppression with methotrexate?

A

leucovorin

96
Q

methotrexate AE’s

A

1) myelosuppresion
2) hepatotoxic
3) mucositis (mouth ulcers)
4) pulmonary fibrosis

97
Q

Bleomycin uses

A

1) testicular cancer

2) Hodgkin lymphoma

98
Q

bleomycin AE’s

A

1) PF
2) skin hyper pigmentation
3) *minimal myelosuppression

99
Q

dactinomycin (actinomycin D) uses

A

1) Wilms tumor
2) Ewing sarcoma
3) Rhabdomyosarcoma
* childhood cancers

100
Q

Doxorubicin, daunorubicin MOA

A

1) generate free radicals

2) intercalate in DNA –> breaks in DNA and decreased replication.

101
Q

Doxorubicin, daunorubicin AE’s

A

1) cardiotoxic (dilated cardiomyopathy)
2) myelosuppression
3) alopecia

102
Q

Busulifan uses

A

1) CML

2) ablating bone marrow before bone marrow transplantation

103
Q

busulfan AE’s

A

1) severe myelosuppression
2) PF
3) hyperpigmentation

104
Q

Cyclophosphamide, ifosfamide MOA and caveat

A
  • Cross-link DNA at guanine N-7.

- require bioactivation by liver

105
Q

What else can you use to prevent hemorrhagic cystitis with cyclophosphamide/ifosfamide?

A

N-acetylcysteine

106
Q

Cyclophosphamide, ifosfamide AE’s

A

1) myelosuppression

2) hemorrhagic cystitis

107
Q

nitrosoureas AE’s

A

CNS toxicity (convulsions, dizziness, ataxia)

108
Q

paclitaxol uses

A

Ovarian + breast carcinomas

109
Q

paclitaxol AE’s

A

1) myelosuppression
2) neuropathy
3) hypersensitivity

110
Q

what are the vinca alkaloids?

A

vincristine, vinblastine

111
Q

vincristine, vinblastine MOA

A

Bind beta-tubulin and inhibit its polymerization into microtubules –> preventing mitotic spindle formation (M-phase arrest)

112
Q

vinca alkaloid used for Hodgkin’s

A

vinblastine

113
Q

vinca alkaloid used for non-Hodgkin’s

A

vincristine

114
Q

Vincristine AE’s

A

1) neurotoxicity (areflexia, peripheral neuritis)

2) constipation (including paralytic ileus)

115
Q

cisplatin, carboplatin uses

A

Testicular + bladder + ovary + lung carcinomas

116
Q

cisplatin AE’s

A

1) nephrotoxicity
2) peripheral neuropathy
3) ototoxicity

117
Q

How do you prevent nephrotoxicity with cisplatin, carboplatin?

A

Amifostine + chloride (saline) diuresis

118
Q

etoposide, teniposide uses

A

testicular + small cell + leukemias/lymphomas

119
Q

etoposide, teniposide AE’s

A

myelosuppression + alopecia

120
Q

irinotecan, topotecan MOA

A

inhibit topoisomerase I, preventing DNA unwinding and replication.

121
Q

irinotecan uses

A

colon cancer

122
Q

topotecan uses

A

ovarian + small cell lung cancers

123
Q

irinotecan, topotecan AE’s

A

severe myelosuppression + diarrhea

124
Q

hydroxyurea MOA

A

Inhibits ribonucleotide reductase, leading to decreased DNA synthesis (S-phase specific).

125
Q

hydroxyurea uses

A

1) melanoma
2) CML
3) sickle cell disease

126
Q

Hydroxyurea AE’s

A

severe myelosuppression

127
Q

How is prednisone/prednisolone used in chemo MOA?

A

Various/bind intracytoplasmic steroid receptor; altering gene transcription.

128
Q

prednisone/prednisolone uses

A

1) CLL

2) non-Hodgkin lymphoma

129
Q

bevacizumab uses

A

Colorectal cancer

RCC

130
Q

bevacizumab AE’s

A

Hemorrhage + blood clots + impaired wound healing

131
Q

Erlotinib MOA

A

EGFR tyrosine kinase inhibitor

132
Q

Erlotinib uses

A

non-small cell lung carcinoma

133
Q

erlotinib AE

A

rash

134
Q

Cetuximab MOA

A

monoclonal antibody against EGFR

135
Q

cetuximab uses

A

Stage IV colorectal cancer (wild-type KRAS), head and neck cancer.

136
Q

cetuximab AE’s

A

Rash + elevated LFTs + diarrhea

137
Q

Imatinib uses

A

Tyrosine kinase inhibitor of BCR-ABL + c-kit

138
Q

imatinib uses

A

1) CML

2) GI stromal tumors

139
Q

rituximab MOA

A

monoclonal antibody against CD20

140
Q

rituximab uses

A

1) non-Hodgkin lymphoma
2) CLL
3) ITP
4) RA

141
Q

rituximab AE

A

Increased risk of progressive multifocal leukoencephalopathy.

142
Q

Tamoxifen and endometrium

A

partial agonist in endometrium, which increases risk of endometrial cancer.

143
Q

raloxifene AE’s

A

Increased risk of thromboembolic events

144
Q

herceptin uses

A

1) HER-2 positive breast cancer

2) gastric cancer

145
Q

perception AE’s

A

cardiotoxic

146
Q

Paraganglioma

A

/rare neuroendocrine neoplasm. /can occur at various body sites (including head, neck, thorax, and abdomen). /usually either asymptomatic or present as a painless mass.

147
Q

blood serum

A

plasma without clotting factors

148
Q

plasma

A

extra cellular matrix of blood cells

149
Q

Which ADP receptor inhibitor is reversible?

A

ticagrelor

150
Q

ribonucleotide reductase

A

Enzyme that catalyzes the formation of deoxyribonucletoides from ribonucleotides, which are in turn used in the synthesis of DNA.

STEP (85 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions