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STEP > Heme Onc Part III > Flashcards

Heme Onc Part III Flashcards

1
Q

Auer rods seen mostly in

A

APL (formerly M3 AML)

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2
Q

Other impt finding in AML

A

Increased myeloblasts on peripheral smear

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3
Q

APL subtype translocation

A

t(15;17)

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4
Q

effect of all-trans retinoid acid?

A

Induces differentiation of promyelocytes.

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5
Q

RF’s for AML

A

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

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6
Q

median age at diagnosis in CML

A

64

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7
Q

Blast crisis

A

CML acceleration and transformation to AML or ALL.

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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.

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9
Q

Burkitt’s translocation

A

8,14

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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.

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11
Q

ALL translocation can rarely be…

A

9;22, BCR-ABL/philadelphia chromosome

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12
Q

Mantle cell activation

A

Cyclin D1

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13
Q

mantle cell translocation

A

11,14

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14
Q

Folicular lymphoma translocation

A

14,18

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15
Q

APL translocation

A

15,17

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16
Q

Langerhans presentation

A

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

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17
Q

Cell markers in langerhans

A

S-100 or CD1a

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18
Q

Chronic myeloproliferative disorder gene association

A

V617F JAK2 mutation

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19
Q

myeloproliferative disorders…

A

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

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20
Q

Causes of relative polycythemia

A

1) dehydration

2) burns

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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

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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

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23
Q

Causes of appropriate absolute polycythemia

A

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

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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

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25
Q

Causes of inappropriate absolute

A

Due to ectopic EPO secretion

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

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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

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27
Q

polycythemia vera etiology

A

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

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28
Q

heparin mechanism

A

Lowers activity of thrombin and factor Xa

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29
Q

what do you need to monitor with heparin?

A

PTT

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30
Q

heparin AE’s

A

Bleeding + thrombocytopenia + osteoporosis

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31
Q

Differences between LMWH and heparin

A

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

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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.

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33
Q

direct thrombin inhibitors

A

bivalirudin

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34
Q

bivalirudin uses

A

1) venous thromboembolism

2) afib

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35
Q

bivaluridin AE’s

A

Bleeding.

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36
Q

How do you treat bleeding associated with bivalirudin?

A

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

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37
Q

Cause of gynecomastia in cirrhosis?

A

Failure of the liver to degrade estrogen.

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38
Q

What is warfarin metabolism affected by?

A

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

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39
Q

What do you need to monitor with warfarin?

A

PT + INR

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40
Q

Warfarin half-life

A

Long

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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.

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42
Q

heparin structure

A

Large, anionic, acidic polymer

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43
Q

warfarin structure

A

small, amphipathic molecule

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44
Q

Heparin site of action

A

blood

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45
Q

warfarin site of action

A

liver

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46
Q

heparin mechanism

A

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

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47
Q

Would heparin or warfarin inhibit coagulation in vitro?

A

heparin, but not warfarin.

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48
Q

PE prophylaxis drug

A

rivaroxaban

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49
Q

Stroke prophylaxis in patients with Afib?

A

Apixaban, rivaroxaban

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50
Q

direct factor Xa inhibitors

A

Apixaban, rivaroxaban

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51
Q

thrombolytics

A

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

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52
Q

thrombolytics labs

A

Increased PT + increased PTT.

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53
Q

thrombolytics contraindications

A

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

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54
Q

thrombolytics bleeding managment

A

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

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55
Q

What are the ADP receptor inhibitors?

A

clopidogrel
prasugrel
ticagrelor (reversible)
ticlopidine

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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.

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57
Q

Drug used for coronary stunting?

A

ADP receptor inhibitors

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58
Q

other uses for ADP receptor inhibitors?

A

1) ACS

2) decrease incidence or recurrence of thrombotic stroke

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59
Q

ticlopidine AE

A

neutropenia

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60
Q

Other AE possible with ADP receptor inhibitors?

A

TTP

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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?

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

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.

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