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Heme Test 2 > Antineoplastic Agents > Flashcards

Antineoplastic Agents Flashcards

1
Q

cyclophosphamide

A

alkylating agent, CCNS

AE: Allopecia and hemorrhagic cystitis, prevented through *Mesna

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2
Q

Ifosfamide

A

alkylating agent, CCNS

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3
Q

busulfan

A

alkyl sulfonate, CCNS

AE: pulmonary fibrosis, hyperpigmentation

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4
Q

cisplatin

A

platinum coordination complex, CCNS

AE’s: renal tubular damage, ototoxicity, Vomiting

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5
Q

methotrexate

A

aka “MTX”

antimetabolite, CCS S phase

  • Inhibits dihydrofolate reductase (DHFR): inhibits conversion of folic acid to tetrahydrolic acid

Indications:
Cancer
Rheumatoid arthritis
Psoriasis

Rescue drug = *Leucovorin

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6
Q

fluorouracil

A

aka “5-fluorouracil; 5-FU”

pyrimidine analog: CCS S-phase

MOA:

  • inhibits DNA synthesis
  • Active compound (FdUMP) covalently binds thymidylate synthetase and blocks de novo synthesis of thymidylate
  • Active compounds (FdUTP and FUTP) are incorporated into both DNA and RNA, respectively
  • *Leucovorin can’t rescue
  • use: colorectal cancer
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7
Q

mercaptopurine

A

aka “6-mercaptopurine; 6-MP”

purine analog: CCS S-phase

MOA:

  • Inhibition of several enzymes of de novo purine nucleotide synthesis
  • Incorporates into DNA and RNA

NOTE: interaction with allopurinol

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8
Q

vinblastine

A

vinca alkaloid: CCS M phase

AE’s: alopecia, myelosupression, neurotoxicity (numbness and tingling of the extremities, loss of deep tendon reflexes, motor weakness, autonomic dysfunction has also been observed)

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9
Q

vincristine

A

vinca alkaloid: CCS M phase

AE’s: alopecia, myelosupression (less than vinblastine), neurotoxicity (numbness and tingling of the extremities, loss of deep tendon reflexes, motor weakness, autonomic dysfunction has also been observed)

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10
Q

paclitaxel

A

taxanes: CCS M phase

AE’s: Hypersensitivity reactions in hands and toes, change in taste

Indicated for treatment of several solid tumors

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11
Q

etoposide

A

epipodophyllotoxin - CCS S-G2 phase

inhibits Type II Topoisomerases, which cut both strands of double-stranded DNA simultaneously to wind and unwind DNA supercoils (CCS - S, G1, G2 phases)

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12
Q

doxorubicin

A

antibiotic: CCNS

MOA:

  1. inhibits Type II Topoisomerases, which cut both strands of double-stranded DNA simultaneously to wind and unwind DNA supercoils (CCS - S, G1, G2 phases)
  2. intercalate DNA
  3. Oxygen free radicals bind to DNA causing single- and double-strand DNA breaks

AE: Free radicals are linked to significant cardiotoxicity
Cumulative cardiac damage can lead to dysrhythmias and heart failure

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13
Q

bleomycin

A

antibiotic anthracenedione: CCS: G2-M phase

MOA: MOA: Free radicals cause single- and double-strand DNA breaks
- Cell cycle specific (G2 arrest)

AE: pulmonary toxicity (5-10%, usually presents as pneumonitis with cough, dyspnea, dry inspiratory crackles)

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14
Q

L-Asparaginase

A

enzyme
CCS - G1 phase

MOA: hydrolyzes circulating L-asparagine into aspartic acid and ammonia, effectively inhibiting protein synthesis

Adverse Effects:

  • Acute hypersensitivity reaction
  • Delayed toxicities include an increased risk of clotting and bleeding, pancreatitis, and CNS toxicity including lethargy, confusion, hallucinations, and coma

indication: targeted for ALL - ALL tumor cells lack the enzyme asparagine synthetase and thus require an exogenous source of L-asparagine

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15
Q

Imatinib

A

protein tyrosine kinase inhibitor: BCR-ABL

The BCR-ABL fusion protein results from the t(9:22) translocation and is found in 95% of patients with CML

Imatinib is a small molecule inhibitor of the ABL tyrosine kinase and has been hailed as a conceptual breakthrough in targeted chemotherapy

Imatinib can also inhibit the RTKs PDGFR and c-KIT

  • see interactions with other drugs that induce the CYP450 system*
  • assoc/ w/ less toxicity than others due to only inhibiting protein tyrosine kinases that are only seen on cancer cells - don’t have as much myelosuppression
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16
Q

Trastuzumab

A

monoclonal antibodies - antigen to tyrosine kinase

** breast cancer tx **

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17
Q

Leucovorin

A

rescue agent - Used to rescue normal cells from high-dose MTX (allows normal cells to continue DNA synthesis)

  • reduced folate can bypass DHFR
  • Antidote for accidental MTX overdose
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18
Q

Mesna

A

rescue agent - prevents hemorrhagic cystitis (attack of bladder lining) - that is associated with cyclophosphamide

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19
Q

Filgrastim

A

G-CSF

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20
Q

Erythropoietin

A

anemia

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21
Q

Ondansetron

A

anti-emesis, serotonin antagonist

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22
Q

-platin

A

platinum coodination complex - alkalating agents

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23
Q

Vin-

A

Vinca alkaloids

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24
Q
  • taxel
A

taxanes

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25
Q

-poside

A

epipodophyllotoxins

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26
Q

-tecan

A

camtothecins

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27
Q

-inib

A

protein tyrosine kinase inhibitor

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28
Q

-zumab

A

monoclonal antibodies

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29
Q

CCS?

A 
antimetabolits - S phase
etoposide = S-G2 phase
Bleomycin = G2-M phase
Taxanes = M phase
Vinca alkaloids = M phase
Camptothecins = S phase
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30
Q

CCNS?

A

Alkalating agents
Antimetabolites
Antitumor antibiotics
Platinum analogs

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31
Q

Growth fraction

A

= the ratio of proliferating cells to resting cells (G0)

Growth fraction is a determinant of responsiveness to chemotherapy

The initial growth rate of most solid tumors is rapid but decreases over time

Cells with high growth fraction:
Bone marrow
GI tract
Hair follicles
Sperm-forming cells

high growth fraction = shorter doubling time (CCS drug)

low growth fraction = longer doubling time (should use CCNS)

Burkitt lymphoma (high growth fraction; curable by chemotherapy) vs. colorectal carcinoma (low growth fraction; chemotherapy has minor activity)

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32
Q

MDR1 gene

A

ATP-dependent transporter gene amplification in neoplasms confers resistance to a broad range of agents used in cancer treatments

The P-glycoprotein is an ATP-dependent efflux pump that actively pumps antineoplastic agents out of cells (MDR1 gene)

Anthracyclines, vinca alkaloids, etoposide, paclitaxel, and dactinomycin

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33
Q

MOA of alkalating agents?

A

form covalent linkages with DNA –> resulting in intrastrand linking and interstrand linking and cross-linking –> prevents unwinding of DNA, results in shut-down of replication process

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34
Q

alkylating agent toxicity?

A

Direct vesicant effects and tissue damage at site of injection (oral administration is of great clinical benefit)

Many alkylating agents produce acute toxicity, such as nausea and vomiting within 30-60 minutes (pretreat with serotonin antagonist)

Delayed toxicities include the common side effects of antineoplastics: bone marrow depression with leukopenia, thrombocytopenia, nephrotoxicity, alopecia, mucosal ulceration, intestinal denudation

35
Q

MOA of antimebolites?

A
  • Structural analogs to compounds necessary for cell proliferation
  • Block or subvert pathways that are involved in, or lead to, cell replication (nucleotide and nucleic acid synthesis)

**Cell cycle specific (S phase)

  1. Folic acid analogs (methotrexate)
  2. Pyrimidine analogs (5-Fluorouracil)
  3. Purine analogs (6-mercaptopurine)
36
Q

allopurinol interactions?

A

Biotransformation of 6-MP includes metabolism to the inactive metabolite 6-thiouric acid by xanthine oxidase (first pass effect in liver)

Allopurinol, a xanthine oxidase inhibitor, is often used as supportive care in the treatment of acute leukemias to prevent hyperuricemia due to tumor cell lysis

Simultaneous administration of allopurinol and oral 6-MP results in increased levels of 6-MP and increased toxicity

Reduce oral 6-MP dose by 50-75%; IV dose unaffected

37
Q

AE’s of antimetabolites?

A

Relatively little acute toxicity after an initial dose

Common toxicities include diarrhea, myelosuppression, nausea, vomiting, immunosuppression, thrombocytopenia, leukopenia, hepatotoxicity

38
Q

MOA of Vinca Alkaloids?

A

Bind to β-tubulin and inhibit microtubule assembly
Cell cycle specific mitosis inhibition (M-phase)

ex: vinblastine, vincristine

39
Q

MOA of Taxanes?

A
  • Bind to β-tubulin and stabilize microtubule assembly
  • Cell cycle specific mitosis inhibition (M-phase)

ex: paclitaxel

40
Q

pulmonary toxicity?

A

bleomycin, busulfan

41
Q

Erlotinib and Gefitinib

A

MOA: Inhibit Epidermal Growth Factor Receptor (EGFR), a receptor tyrosine kinase

**Preferred single-agent first-line therapy for NSCLC patients with somatic activating EGFR mutations

AE: Produce dermatologic toxicities

42
Q

tyrosine kinases action?

A

When mutated, overexpressed, or structurally altered, tyrosine kinases can become potent oncoproteins

Abnormal activation of tyrosine kinases has been found in many human neoplasms

Aberrant tyrosine kinase activity can occur in receptor tyrosine kinases or cytoplasmic kinases –> promoting survival, proliferation and growth

Intracellular (nibs) vs. extracellular (mabs)

43
Q

ototoxicity?

A

Cisplatin

44
Q

Mucositis?

A

methotrexate, melphalan

45
Q

Cardiotoxicity?

A

doxorubicin, daunorubicin

46
Q

peripheral neuropathy?

A

vincristine

47
Q

pulmonary fibrosis?

A

bleomycin, busulfan

48
Q

nephrotoxicity?

A

cisplatin, cyclophsophamide

49
Q

hemorrhagic cystitis?

A

cyclophsophamide, ifosfamide

50
Q

12 y/o male evaluated in hematology clinic b/c of fatigue and peripheral blood eos, presents with intermittent cramping, pain in arms and legs and anterior c/p thats worse with mvmt, deep breathing, coughing - HR is 120, palpable lymph nodes in inguinal regions - bippsy shows marked hypercellular with eos and erythroid elements, amid clusters of blasts with irregular nuclei. blood smear shows leukocytosis with marked eos. Cytogenetic FISH analysis shows t(15;14) - pt. ddx with ALL . cell cycle specific manner?

A

antimetabolites: mercaptopurine, methotrexate, fluorouracil

51
Q

which agent is administered with high dose MTX to rescue healthy cells?

A

leucovorin - bypasses dihydrofolate reductase (enzyme inhibited by MTX) in the cycle and enters in later, results in production of nucleotide precursors in normal cells

52
Q

66 y/o female with CBC drawn during her annual physical shows WBC count of 60,000 and 90% neutrophils, hematocrit of 32%, platelet count of 300,0000. only pertinent PE is splenomegally. Has AML… with t(9;22), phildadelphia chromosome, BCR-ABL. which drug to use? assuming mutation has occurred in BCR-ABL fusion protein, which agent is best to use?

A

BCR-ABL results in unregulated tyrosin kinase activity, implictated in malignant transformation due to effects on cell cycle, inhibition of apoptosis and increased proliferation of cells -

  1. use Imatinib - a protein tyrosine kinase inhibitor which inhibits BCR-ABL kinase
  2. Dasatinib - it inhibits BCR-ABL also used when there is resistance to Imatinib
53
Q

Her2/neu positive?

A

trastuzumab - monoclonal antibodies

continued cancer growth after remission would be due to? drug resistance

54
Q

deferoxamine?

A

antidote for iron poisoning

55
Q

N-acetylcsteine?

A

antidote for tyelonl

56
Q

Vit K?

A

antidote for coumadin/warfarin

57
Q

CCNS? acts by intercalating into DNA strands?

A

doxorubicin (doesn’t actually bind to the DNA, not a covalent bond)

alkylating agents (include cyclophosphamide and ifossfamide) form COVALENT bonds with the DNA

however BOTH prohibit DNA from unwinding and are CCNS

58
Q

mechlorethamine?

A

alkylating agent - it alkylates DNA, causing cross-links b/w parallel DNA strands

59
Q

most likely condition for which methotrexate is given other than cancer?

A

rheumatoid arthritis

60
Q

antimetabolites?

A

CCS- inhibit S phase

5-Fluorouracil
6-Mercaptopurine
Methotrexate

61
Q

epipodophyllotoxins?

A

CCS: S-G2 phase through inhibiting topoisomerase II
*natural product

ex. Etoposide

62
Q

Antitumor antibiotics?

A

CCS: G2-M phase
* natural product

ex. Bleomycin

63
Q

Taxanes?

A

Mphase: stabilze MT’s by binding to Beta tubulin

ex. Paclitaxel

64
Q

Vinca Alkaloids?

A

Natural product
M phase, by inhibiting microtubule assembly

ex. Vinblastine, vincristine

65
Q

Alkylating agents?

A

CCNS

ex. Cyclophosphamide, Ifosfamide, Busulfan, Cisplatin

66
Q

Anthracyclines?

A

CCNS, in the natural class of antibiotics

ex. Doxorubicin

67
Q

tx of CML with, BCR-ABL

A

Imatinib

68
Q

NSCLC?

A

Gefitinib, erlotinib

69
Q

treatment of CML resistant to imatinib

A

Dasatinib

70
Q

HER2/Neu

A

Trastuzumab

71
Q

Which of the following effects are anticipated in response to imatinib therapy

A

Interactions with other drugs that induce the CYP450 system

72
Q

Rituximab

A

CD20, Non-Hodkins lymphoma

73
Q

Alemtuzumab

A

CD52, chronic lymphocytic luekemia

74
Q

Gemtuzumab

A

CD33, AML

75
Q

Cetuximab

A

EGFR (ErbB-1)

colorectal, lung, pancreatic, breast

76
Q

Bevacizumab

A

VEGF, Colorectal cancer, lung

77
Q

trastuzumab?

A

watch out for cardiac toxicity

78
Q

Ibratumomab/Tositumomab

A

CD20, NLH

79
Q

CD20, nonhodkins lymphoma

A

use rituximab

OR

Ibritumomab, Tositumomab

80
Q

which causes problems with CNS?

A

Asparaginase and Cytarabine

81
Q

CD52

A

chronic lymphocytic leukemia, Alemtuzumab

82
Q

CD33

A

AML, Gemtuzumab

83
Q

EGFR (ERB-1)

A

Colorectal, lung, pancreatic, breast cancer - Ceftuximab

84
Q

VEGF

A

Colorectal, lung cancer

- Bevacizumab

Heme Test 2 (4 decks)

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