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CMOD > Sweatman Cytotoxic Chemotherapy Agents > Flashcards

Sweatman Cytotoxic Chemotherapy Agents Flashcards

1
Q

3 majors MOA’s through which Chemotherapy drugs work

A
  1. Action on DNA
  2. Action on Mitotic Spindle
  3. Hormonal Agents
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2
Q

Action on DNA can be broken up into (2)

A
  1. damage to DNA

2. inhibition of DNA synthesis

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3
Q

Action on mittotic spindle can be further subdivided into (1)

A

Microtubule Inhibition

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4
Q

Hormonal agents can be broken up into (2)

A
  1. agonists (prednisone)

2. antagonists (tamoxifen)

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5
Q

Most toxic pharmaceutic agents

A

anti-cancer drugs

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6
Q

DNA damage can be subdivided into 2 types

A
  1. alkylation (cyclophosphamide)

2. free radical formation (doxorubicin)

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7
Q

Inhibition of DNA synthesis or function can be divided into two categories

A
  1. Antimetabolites (methotexate)

2. Topoisomerase (etoposide)

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8
Q

Anti-cancer drugs that target cells undergoing cycling

A

Cell-Cycle Specific drugs (CCS)

*cannot kill drugs that are in the G0 phase

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9
Q

Anti-Cancer drugs that kill tumor cells in both the cycling and resting phases

A

Cell-Cycle Non-Specific (CCNS)

*can kill cells which are in G0 phase

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10
Q

CCS drugs are particularly effective when

A

larger proportion of cells within a tumor are proliferating (cycling)

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11
Q

Fraction of cells within a tumor hat are actively dividing

A

Growth fraction

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12
Q

Log-Kill hypothesis

A

Chemotherapeutic agents work via First order kinetics–> a constant proportion of cells are killed per log-dose, NOT a constant NUMBER of cells.

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13
Q

1 log dose will decrease the tumor cell population by

A

one order of magnitiude (90%)

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14
Q

rescue therapy

A

administration of endogenous metabolites to counteract the effects of anticancer drugs on normal tissues

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15
Q

Vesicant example

A

mechloethamine (an alkylating agent)

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16
Q

Vesicant definition

A

drugs that causes blisters when it contacts tissues–> damaging to the veins if administered in high enough concentrations into small vessels…

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17
Q

M phase inhibitors

A

Vinca Alkyloids

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18
Q

G2 phase inihibotor

A

Bleomycin

and podophyllotoxins

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19
Q

G2 and S phase inhibitors

A

Podophyllotoxins

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20
Q

S phase inhibitors

A

Methotrexate

and Podophyllotoxins

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21
Q

Resistance mechanism especially important for alkylating agents

A

Increased DNA repair

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22
Q

MOR important to Bleomycin, CIsplatin, and Anthracyclins

*all of which form electrophillic species

A

Formation of trapping agents

–>increase production of thiol trapping agents which interact with these drugs

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23
Q

MOR important to Methotexate

A

Change in target enzyme
and Increased synthesis of enzyme
*DHFR

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24
Q

examples of purine antimetabolites

A

mercaptopurine

thioguanine

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25
Q

pyrimidine antimetabolites

A

cytarabine

flourouracil

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26
Q

MOR involving purine/pyrimidine antimetabolites

A

> decreased activity of tumor cell enzymes to CONVERT PRODUGS INTO CYTOTOXIC METABOLITES

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27
Q

another MOR involving puring/pyrimidine antimetabolites

A

Increased inactivation of these prodrugs results in decreased effect

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28
Q

MOR involving many Anti-cancer drugs

A

decreased drug accumulation/increased efflux

> upregulation of MDR1 (pGP)

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29
Q

Alkylating agents are CCS or CCNS?

A

CCNS

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30
Q

Alkylating agents MOA

A

–>form reactive molecular species that alkylate nucleophillic groups on DNA, particularly N-7 position of guanine–>leads to CROSS LINKING, ABNORMAL BASE PAIRING AND DNA BREAKAGE

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31
Q

RESISTANCE TO ALKYLATING AGENTS OCCURS VIA

A

INCREASED DNA REPAIR MECHANISMS
DECREASED DRUG PERMEABILITY
PRODUCTION OF TRAPPING THIOLS

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32
Q

nitrogen mustards (alkylating agents)

A

cyclophosphamide

mechlorethamine (a vesicant)

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33
Q

CYP450 break down of cyclophosphamide results in

A

acrolein ( a breakdown product)

CYP450 break down is required for anti-tumor capabilities

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34
Q

Hemorrhagic Cystitis is brought on by ________ and releived by ____________.

A

acrolein build up following cyclophosphamide tx

mesna and intense hydration

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35
Q

biotransformation of cyclophosphamide takes place in the

A

liver with CYP450’s

36
Q

Conversion of Mechlorethamine takes place

A

spontaneously in the body to a cytotoxic product

37
Q

Drug with marked vesicant actions

A

Mechlorethamine

38
Q

Alkylating agents: Platinum analogs

A

Cisplatin–>testicular carcinoma, bladder, lung ovary
carboplatin–>similar to cisplatin
oxaliplatin–> colon

39
Q

side effect of cisplatin

A

tinnitus–> acoustic nerve damage

40
Q

Alkylating agents: procarbazine characteristics

A

reactive agent that formd hydrogen peroxide–> generates free radicals–> DNA strand scission

41
Q

ROS producing cemotherapeutic agent

A

procarbazine

42
Q

Anti cancer agent with disulfram-like reactions–> and therefore should not be taken with alcohol

A

procarbazine

*aldehyde dehydrogenase inhibitor

43
Q

used to reat chronic myelogenous leukemia

A

Bisulfram–> an alkylating agent

44
Q

Antemetabolites are CCS or CCNS

A

CCS

45
Q

Antimetab. antagonist of folate

A

methotrexate

46
Q

Antimetab. antagonist of purines

A

mercaptopurine

thioguanine

47
Q

Antimetab. antagonist of pyrimidines

A

flourouracil
cytarabine
gemcitabine

48
Q

Antimetabolites primarily work on the ______ phase

A

Synthesis phase

49
Q

Down side of antimetabolites

A

immunosupressant

50
Q

MOA for methotrexate

A

substrate for and inhibitor of DHFR
*ultimately leads to decrease in the synthesis of THYMIDYLATE, PURINE NUCLEOTIDES, AND AMINO ACIDS
(INTERFERES WITH NUCLEIC ACID AND PROTEIN METABOLISM

51
Q

important product derived from breakdown of methotrexate that leads to cytotoxicity–>

A

polyglutamate derivatives

52
Q

does methotrexate reach CNS

A

NO–> but good distribution everywhere else

53
Q

clearance of methotrexate–>

A

renal, requires good hydration

54
Q

toxic effects of methotrexate (bone marrow, skin, gi) can be countered by what?

A

leucovorin rescue–> folinic acid

55
Q

6-MP and ^-TG are activated by

A

hypoxanthien-guaninephosphoribosyl transferases
HGPRTases–> to toxic nucleotides that inihibit several enzymes involved in purine metabolism
–> resistant tumors have DECREASED HGPRTase activity

56
Q

Bioavailability of 6-MP and 6-TG

A

poor due to first pass metabolism

57
Q

This drug results in thymine-less death

A

5 FU–flourouracil

–>inhibits thymidylate synthase

58
Q

Does 5-FU distribute to the cerebrospinal fluid

A

yes, when given IV

59
Q

inihibitor of DNA polymerase

A

Cytarabine (ARA-C)

60
Q

Of all antimetabilites–> this one is the most specific for the S phase

A

Cytarabine

61
Q

deoxycytidine analog that when converted to active diphosphate form inihibits riboneucleotide reductase–> deminishing pool of deoxyribonucleotides–> no DNA synthesis

A

Gemcitabine

62
Q

Plant alkaloids are CCS or CCNS

A

CCS

63
Q

Name the types of plant alkaloids

A

vinca alkaloids
podophyllotoxins
camptothecins
taxanes

64
Q

name the vinca alkaloids

A

vinlablastine

vincristine

65
Q

name the podophyllotoxins

A

etoposide

teniposide

66
Q

name the camptothecins

A

topotecan

irinotecan

67
Q

name the taxanes

A

paclitaxel

docetaxel

68
Q

VInca alkyloids MOA

A

block the formation of mitottic spindle by preventing the assembly of tubulin dimers into microtubules

69
Q

vinca alkylioids act primarily in what phase

A

M phase

70
Q

clearance of vinca alkyloids

A

billiary excretion

71
Q

MOA for etoposide

A

increases degradation of DNA via interaction with topo II

*also inhibits mitochondrial electron transport chain

72
Q

when are podophyllotoxins most active

A

late S early G2

73
Q

MOA for topotecan and irinotecan (campothectins)

A

inhibit topo I, damage DNA by inihiting an enzyme tha religates single DNA strands during normal DNA repair processes

74
Q

Pharmacokinetics or irinotecan ( a campothectin)

A

prodrug converted to its active form in the liver

topotectan–> eliminated renally
irinotecan–> eliminated in the bowel and feces

75
Q

How to taxanes work

A

interfere with mitotic spindle –> prevents MICROTUBUILE DISSASSEMBLY INTO TUBULIN DIMERS

76
Q

HOW IS PACLITAXEL AND DOCETAXEL ADMINISTERED

A

IV

77
Q

NAME THE ANTHRACYCLINS

A

doxorubicin

daunorubicin

78
Q

MOA for doxorubicin (anthracyclin)–>

A

intercalate bw base pairs, inhibit topo II and generate free radicals–> block synthesis of RNA and DNa and cause DNA strand breakage

79
Q

anti cancer drugs causing increased free radicals

A

procarbazapine and doxorubicin, daunorubicin, belomycin

80
Q

Anthracyclins are CCS or CCNS

A

CCNS

81
Q

Main toxicity associated with doxorubicin

A

cardiac toxicity–> EKG changes and possible arrhythmia–> cardiomyopathy and CHF

82
Q

drug administered to counteract cardiac toxicity of doxorubicin

A

dexrazoxane–> inhibits iron mediated free radical generation

83
Q

Belomycin MOA

A

mixture or GlycoPep’s that make free radicals which bidn to DNA and cause strand breakage and inhibit DNA synthesis

84
Q

Belomycin works mostly in which phase

A

G2

85
Q

CCNS drugs that bind to dsDNA and inhibit DNA-dependent RNA synthesis

A

dactinomycin–> must be given parenterally–> in tact drug and metabolites are excreted in the bile

86
Q

CCNS drug that is metabolized by the liver to form an alkylating agent that cross-links DNA

A

MITOMYCIN

87
Q

ALL these drugs cause bone marrow suppression except

A

Belomycin
Vinblastine
VIncristine

CMOD (19 decks)

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