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Year 2 Heme lymph > DSA antineoplastic agents, Linger, Part II > Flashcards

DSA antineoplastic agents, Linger, Part II Flashcards

1
Q

What are the 5 major types of alkylating agents

A

nitrogen mustards, methylhydrazines, alkyl sulfonates, nitrosoureas, triazenes
and dNA platinum compounds

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2
Q

MOA alkylating agents

A

form covalent bonds with DNA and alkylate it leading to intra and inter-strand corss lnking to prevent tumor from unwiding DNA for mRNA production

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3
Q

which cells are most susceptible to alkylating agents

A

cells that are replicating

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4
Q

alkylating agents

cell cycle specific or non?

A

nonspecific

though late G1 and S phase most susceptible

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5
Q

Which drug group has direct vesicant effects that can dmaage tissue at sits of injection

A

alkylating agents

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6
Q

systemic toxicities of alkylating agents

A

dose related and occur in rapidly growing tissues like bone marrow, GI tract and repro system

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7
Q

what are acute toxicity Sx of alkylating agents and preTx to avoid the Sx?

A

nausea and vomiting within 30-60 min IV administration

pretreat with odansetron

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8
Q

what are the delayed toxicities of alkylating agents

A

BM depression with leukopenia, thrombocytopenia, nephrotoxicity, alopecia, mucosal ulceration and intestinal denudation

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9
Q

what must you do if administering alkylating agent

A

monitoring blood counts to watch for leukopenia and thrombocytopenia

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10
Q

alkylating agents increase risk for what

A

secondary malignancies

AML

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11
Q

adverse effects cyclophosphamide

A

hemorrhagic cystitis from accumulation of acrolein

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12
Q

Tx for adverse effects of cyclophasphamide

A

mesna, sulfhydryl compound that reacts and neutralizes acrolein in acid environment in urinary tract

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13
Q

what are adverse effects of cisplatin

A

nephrotoxicity
ototoxicity- tinnitus and hearing loss of high freq range, unilateral or bilaterl
nausea and vomiting

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14
Q

how do we overcome nephrotoxicity from cisplatin administration

A

routine hydration and diuresis

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15
Q

adverse effect busulfan

A

hyperpigmentation, pulmonary fibrosis and adrenal insufficiency

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16
Q

Main categories of antimetabolites

A

folic acid analogs, pyrimidine analogs, purine analogs and related inhibitors

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17
Q

What is the main folic acid analog

A

methotrexate

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18
Q

MOA methotrexate

A

inhibits dihydrogolate reductase and blocks conversion folic acid to tetrahydrofolic acid which is needed to make thymidylate, purines, serine and methionin

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19
Q

low dose methotrexate is common Tx for what

A

RA colitis, psoriasis, some cancers

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20
Q

high dose methotrexate therapy enters cells how

A

healthy cells via diffusion across concentration gradient causing injury to healthy tissues

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21
Q

what is the resuce drug for methotrexate

A

leucovorin because allows thymidylate synthesis to continue

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22
Q

is methotrexate cell cycle spceific or non

A

cell cycle specific S phase

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23
Q

adverse effects methotrexate

A

mucositis, diarrhea, myelosuppression with neutropenia dn thrombocytopenia, nausea, vomiting, immunosuppression, hepatotoxicity, fatigue

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24
Q

What drugs are pyrimidine analogs

A

Fluorouracil (5-FU)

cytarabine (Ara-C)

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25
Q

MOA fluorouracil

A

covalently binds to thymidylate synthestase and blocks synthesis
also incorporated into DNA and RNA interfering with synthesisis, function , processing and mRNA translation

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26
Q

most widley used in colorectal cancer

A

5-FU

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27
Q

is 5-FU cell cycle specific or non

A

cell cycle specific S phase

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28
Q

adverse effects 5-FU

A

anorexia, nausea, stomatitis, diarrhea

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29
Q

MOA cytarabine

A

competetively inhibits DNA polymerase alpha and beta blocking synthesis and repair

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30
Q

is cytarabine cell cycle specific or non

A

cell cycle specific S phase

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31
Q

What do we use cytarabine for

A

hematologic malignancies

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32
Q

main adverse effects cytarabine

A

myelosuppression, mucositis, nausea, vomiting and neurotoxicity at high doses

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33
Q

What are the purine analogs and MOA

A

Mercaptopurine

inhibits purine NT synthesis and DNA and RNA synthesis because if triphosphate incorporation

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34
Q

is mercaptopurine cell cycle spcific or non

A

cell cycle specific S phase

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35
Q

what drug should you not use with allopurinol because increased toxicity

A

mercaptopurine

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36
Q

adverse effects mercaptopurine

A

myelosuppression, immunosuppression, hepatotoxicity

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37
Q

MOA thioguanine

A

inhibits NT synthesis and DNA and RNA synthesis due to triphophate incorporation

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38
Q

what drug CAN you use will full dose allopurinol that still inhibits DNA

A

thioguanine

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39
Q

What are the antimitotic drugs

A

vinca alkaloids and taxanes

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40
Q

what are the vinca alkaloids

A

vinblastine and vincristine

41
Q

MOA of the drug derived form madagascar periwinkle plant

A

bind to beta tubulin and inhibit microtubule assembly
(inhibits mitosis)
vinblastine and vincristine

42
Q

Drug resistance to vinca alkaloids

A

from membrane efflux pump P glycoprotein

43
Q

adverse effects of the vinca alkaloids

A

hair loss, local cellulitis if extravasated

myelosuppresion- vinblastine

44
Q

which vincalkaloid causes more neurological toxicities

A

vincristine

numbness and tingling of the extremities and loss of DTR followed by motor weakness

45
Q

what are the taxanes

A

paclitaxel and docetaxel

46
Q

MOA of drug derived from western yew tree

A

binda beta tubulin and promotes microtubule formation and stabilization (prevents mitosis)
taxanes

47
Q

adverse effects paclitaxel

A

bone marrow depression and peripheral sensory neuropathy

48
Q

docetaxel

A

neurotoxicity, fluid retention, neutropenia

49
Q

what are the epipdophyllotoxins

A

etoposide and teniposide

50
Q

MOA epipodophyllotoxins

A

inhibit topoisomerase II leading to DNA damage through strand breakage induced by formation of drug complex with DNA and enzyme

51
Q

What are the camptothecin analogs

A

topotecan andirinotecan

52
Q

MOa camptothecin analogs

A

inhibit activity of topoisomerase I resulting in DNA damage and blockade of DNA replication and trascription

53
Q

are camptothecin analogs cell cycle specific or non

A

cell cycle specific

54
Q

adverse effects camptothecin analongs

A

bone marrow depression, diarrhea, nausea and vomiting

55
Q

Tx for early diarrhea from captothecin analogs? late diarrhea Tx?

A

early- atropine

late- need electrolyte and fluid replacement

56
Q

What are the tyeps of antitumor Ab

A

anthracyclines, dactinomycin, bleomycin and mitomycin

57
Q

what are the anthracyclines and MOA

A

doxorubicin
daunorubicin
-inhibit topoisomerase II
-intercalate DNA and block synthesis of DNA and RNA and blocks DNA strand scission
-generates semiquinone and ROS
-binds to cellular membranes to alter fluidity and ion transport

58
Q

how do anthracyclines lead to cardiotoxicity

A

release of O2 species

59
Q

are antrhacyclines cell specific or non

A

non because intercalation of DNA

60
Q

Adverse effects anthracyclines

A

nausea, red urine!, alopecia, myelosuppression, stomatitis, cardiotoxicity

61
Q

MOA bloemycin and is it cell specific?

A

binds DNA causing single and ds breaks
inhibits DNA biosynthesis
cell cycle specific G2

62
Q

adverse effects belomycin

A

pulmonary toxicity dose limited
pneumonitis, cough, dyspnea, dry inspiratory crackles, infiltrates on CXR
allergic rxns
fever, hypotension, skin toxicity, mucositis and alopecia

63
Q

MOS dactinomycin

A

binds to ds DNA and intercates between guanine-cytosine base pairs which prevents DNA dependent RNA polymerase from transcribing RNA

64
Q

adverse effects dactinomycin

A

anorexia, nausea, vomiting
long term: alopecia, BM depression, stomatitis, increased inflammation and pigmentation in areas previously subjected to Xray radiation

65
Q

what are the groups of natural antineoplastic agents

A 
antimitotic
epipodophyllotoxins
camptothecin analogs
antitumor Ab
enzymes
66
Q

what enzymes are natural antineoplastic agents

A

asparaginase and pegaspargase

67
Q

MOA asparaginase and pegaspargase

A

hydrolyzes circulating L asparagine to aspoartic acid and ammonia
(inhibits protein synthesis)

68
Q

what has longer half life

asparaginase and pegaspargase

A

pegaspargase

69
Q

are asparaginase and pegaspargase cell cycle specific

A

yes G1

70
Q

Which tumors are vulnerable to asparaginase and pegaspargase

A

ALL tumor cells because lack asparagine synthetase and need exogenous source L asparagine

71
Q

adverse effects asparaginase and pegaspargase

A

acute HS reaction: fever, chills, nausea, vomiting, skin rash, urticaria
delayed toxicities:inc risk clotting and bleeding, pancreatitis and CNS toxicity:lethargy, confusion, hallucinations and coma

72
Q

what are the steroids used forcancer and why

A

antilymphocytic effects

oral: prednisone, hydrocortisone, dexamethasone
topical: clobetasol, diflorasone, halobetasol, betamethasone

73
Q

MOA hydroxyurea

A

inhibits ribonucleoside diphosphate reductase

S cell cycle specific

74
Q

What drug is used for acute promyelocytic leukemia

A

tretinoin because induces clonal proliferation or granulocytic differentiation

75
Q

adverse effects tretinoin

A

Vit A toxicity, retinoic acid syndrome, increased cholesterol and TGs
CNS toxicity
GI disturbances

76
Q

What is used to treat progressive persistent or reccurent cutaneous T cell lymphoma

A

vorinostat

77
Q

MOA imatinib

A

inhibits tyrosine kinase domain of Bcr-Abl and prevents phosphorylation
also inhibits kinases PDGFR, stem cell factor and c-kit

78
Q

what is imatinib used to Tx

A

CML

GI stromal tumors with c-kit

79
Q

which protein tyrosine kinase inhibitor should be used with caution with drugs that interact with CYP3A4

A

imatinib

80
Q

adverse effects imatinib

A

myelosuppression, fluid retention with ankle and periorbital edema, diarrhea, myalgias

81
Q

MOA dasatinib

A

kinase inhibitor Bcr-Abl, c-kit and PDGFR-beta

82
Q

MOA Nilotinib

A

inhibits Bcr-Abl, c kit and PDGFR-beta with higher affinity for Abl
Imatinib resistance

83
Q

What are the inhibitors of Epidermal EGFR

A

erlotinib and gefitinib

84
Q

MOA sorafenib and sunitinib

A

multikinase inhibitor

inhbits intracell Rag kinases and surface kinases R like VEGFR

85
Q

drug used to inhibit Her2/neu that is less cardiotoxic than trastuzumab

A

lapatinib

86
Q

MOA bortezomib

A

inhibits proteosomes, activating signaling cascades that lead to cell cycle arres and apoptosis

87
Q

what is bortezomib used for

A

multiple myeloma

or refractory mantle cell lymphoma

88
Q

What is IL-2 used for

A

stimulate proliferation activated T cells and secretion NK cytokines to increse cytotoxic killing

89
Q

What are first line drugs in post-transplant immunsuppression? and MOA

A

temsirolimus and everolimus

inhibit mTOR R causing immunosuppression

90
Q

MOA rituximab

A

against CD20 on normal and malignant B lymphocytes causing C’mediated lysis and Ab-dependent cellular cytotoxicity and induction apoptosis

91
Q

What is rituximab used to Tx

A

low grade follicular CD20+, B cell non-hodgkin lymphoma and Tx DLBCL20+
RA with methotrexate

92
Q

adverse effects rituximab

A

cytopenia, HS reactions

93
Q

What monoclonal Ab is approbed for Tx B cell CLL?

A

alemtuzumab

94
Q

gemtuzumab used to Tx?

A

AML

95
Q

MOA trastuzumab and what is it used to Tx

A

binds Her2/neu R that is on 25-30% breast cancers and inhibits intracell signaling events and neoplastic prliferation

96
Q

adverse effects trastuzumab

A

cardiotoxicity, ventricular dysfunction- should be discontinued if dec in L ventricular function

97
Q

what is used to Tx refractory or relapsed low grade NHL or follicular B cell NHL

A

ibritumomab

98
Q

Gardasil prevents what

A

HPV 16 and 18 strains

and 6 and 11– genital warts

Year 2 Heme lymph (28 decks)

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