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pathophysiology > chemo quiz 1 > Flashcards

chemo quiz 1 Flashcards

1
Q

chemotherapy

A

treatment of cancer involving the administration of one or more anti-cancer drugs

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2
Q

chemotherapy drugs exhibit

A

systemic toxicity

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3
Q

what is systemic toxicity

A

they affect all cells in the boy (some ore than others)

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4
Q

what are the types of chemo

A

drugs that stop the formation of new DNA by impending creation of its building blocks

drugs that damage or bind to existing DNA so it can’t be correctly copied

drugs that impede mitotic spindle from forming

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5
Q

components of DNA

A

phosphate
sugar backbone (deoxyribose )
nitrogenous bases

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6
Q

nitrogenous bases

A

purines and pyrimidines

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7
Q

purines

A

A and G

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8
Q

pyrimidines

A

C and T ( and U )

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9
Q

without phosphate and nitrogenous bases

A

we can’t make DNA… the cell has to find ways to build each of these building blocks

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10
Q

many chemotherapeutic drugs

A

try to stop cell from forming building blocks of dna

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11
Q

purine production

A

carbon and nitrogens inside come from amino acids

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12
Q

exceptions in synthesis of purines

A

carbons labeled 2 and 8 are pulled from folic acid

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13
Q

another name for folic acid

A

folate

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14
Q

purines look like

A

bigger&raquo_space; 2 rings

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15
Q

pyrimidines look like

A

smaller&raquo_space; 1 ring

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16
Q

does the body use folate in its natural form to make purines

A

no&raquo_space;> first need to be converted into

tetrahydrofolate

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17
Q

enzyme that turns folate and tetrahydrofolate

A

folic acid reductase

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18
Q

THF

A

tetrahydrofolate

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19
Q

without folic acid reductase

A

no THF… purines can’t be synthesized

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20
Q

one of oldest chemotherapeutic drugs

A

methotrexate

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21
Q

what does methotrexate do

A

stop the production of purines A and G

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22
Q

methotrexate’s chemical structure

A

very similar to that of folic acid

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23
Q

methotrexate is so similar to folic acid that

A

folic acid reductase would rather bind to it than folic acid

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24
Q

what is different between folic acid and methotrexate

A

CH3

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25
Q

methotrexate is a ______ of ______

A

competitive inhibitor of folic acid reductase

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26
Q

why is methotrexate a competitive inhibitor of folic acid reductase

A 
it
has the same
shape (of folic acid) and
competes for
the active site
in the enzyme.
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27
Q

inhibitors

A

drugs that stop enzymes from doing jobs

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28
Q

types of inhibitors

A
  • Competitive inhibitors
  • Noncompetitive inhibitors
  • Uncompetitive inhibitors
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29
Q

competitive inhibitors

A

compete for the binding site

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30
Q

if the competitive inhibitor is there

A

the substrate cannot bind

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31
Q

noncompetitive inhibitors

A

do not compete… they bind elsewhere

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32
Q

if the noncompetitive inhibitor is there

A

substrate can still bind to the

enzyme, but the reaction does not occur.

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33
Q

in uncompetitive inhibitor……..

A

the substrate

MUST bind first.

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34
Q

after substrate binds first in uncompetitive inhibitors

A

the inhibitor will bind to the complex and stop reaction from happening

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35
Q

uncompetitive inhibition will generally

A

trap the substrate inside, too!

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36
Q

when Folic acid reductase and methotrexate stick to each

other……

A

folic acid reductase’s binding site is now full, it will never make THF

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37
Q

if there is no THF….

A

This means the cells can’t produce purines anymore.

This means the cells can’t produce DNA anymore.

This means DNA replication can’t happen

this means mitosis can’t happen&raquo_space;> gg cancer

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38
Q

when THF isn’t made the cell’s original dna …

A

original, inherited DNA is still fine

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39
Q

5-FU

A

5-Flurouracil

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40
Q

5-FU also called

A

adrucil

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41
Q

5-FU is a

A

pyrimidine synthesis inhibitor

42
Q

specifically 5-FU stops synthesis of

A

thymine

43
Q

thymine is made

A

from uracil in many steps

44
Q

one of most important steps of making thymine from uracil

A

conversion of dUMP into dTMP

45
Q

dUMP to DTMP conversion is catalyzed by

A

enzyme thymidylate synthase

46
Q

thymidylate synthase prefers

A

binding to breakdown product of 5-FU rather than dUMP

47
Q

what breakdown product does thymidylate synthase prefer binding to

A

FUMP

48
Q

when thymidylate synthase binds and sticks to FUMP

A

dTMP is not synthesized, thymine is not synthesized

49
Q

result of dTMP is not synthesized….

A

thymineless death

50
Q

what is a drug that falls into category of chemotherapeutic drugs that damage or bind to existing DNA so it can’t be copied

A

cisplatin

51
Q

what happens when cisplatin enters cells

A

two chlorine groups grab onto an atom

52
Q

when cisplatin enters cells its two chlorine groups grab onto what atom

A

the 7th nitrogen of guanine groups

53
Q

when cisplatin 2 chlorine groups bind to 7th nitrogen of guanine groups

A

forms cross-links between them, causes the DNA to fold into unusual shapes

54
Q

what type of cross-linkages can cisplatin cause

A

inter-strand or intra-strand cross-linkages

55
Q

what happens in both intra-strand and inter-strand cross-linkages

A

the double helix DNA becomes warped and p53 detects DNA damage

56
Q

when p53 detects DNA damage

A

leads to apoptosis

57
Q

cisplatin is what based

A

platinum

58
Q

other platinum based drugs are…

A

carboplatin

oxaliplatin

59
Q

other platinum-based drugs cause

A

cross-linkages , end in platin

60
Q

what works to form a different kind of cross-linkage between nucleotides

A

alkylating agents

61
Q

how do alkylating agents work

A

instead of using platinum they add an alkyl group

62
Q

what is an alkyl group

A

a nitrogen with a chain of carbons on each side

63
Q

like-platinum based drugs, alkylating agents attach to

A

the 7th nitrogen of guanines

64
Q

many alkylating agents fall

A

fall into a class of molecule that mimic mustard gas

65
Q

what are alkylating agents that fall into a class of molecule that mimic mustard gs

A

nitrogen mustards

66
Q

what is the most common nitrogen mustard

A

cyclophosphamide

67
Q

anthracyclines

A

another class of chemotherapeutics

68
Q

unique mechanism of anthracyclines

A

INTERFERE with the function of DNA topoisomerase II

69
Q

as dna is used

A

it gradually coils up more and more

70
Q

as dna coils up,what need to be released

A

torsional stress on the molecule needs to be released

71
Q

DNA topoisomerase function

A

release torsional stress on DNA

72
Q

how does DNA topoisomerase do its job

A

creates a small “nick” in DNA coils, untwists the DA, and then repair the nick

73
Q

if the stress in DNA does not get repaired (by DNA tpoisomerase)

A

the DNA is eventually damaged and the cell will die

74
Q

Anthracyclines generally have names that…..

A

end in rubicin

75
Q

important anthracyclines

A

doxorubicin, daunorubicin, and epirubicin

76
Q

what are the drugs that damage to bind to existing DNA so it can not be copied

A

cisplatin (platin)
alkylating agents
anthracyclines (rubicin)

77
Q

drugs that stop the formation of new DNA by impeding the creation of its building blocks

A

methotrexate

adrucil (5-FU or 5-Fluorouracil)

78
Q

mitotic spindle

A

integral part of cell division

79
Q

fibers in the mitotic spindle are made of

A

microtubules `

80
Q

what do fibers do in the mitotic spindle

A

grab onto chromosome pairs and pull them apart

81
Q

without the mitotic spindle

A

cell division cannot happen

82
Q

what are microtubules made of

A

two proteins

83
Q

what 2 proteins are micotubules made of

A

alpha-tubulin , beta-tubulin

84
Q

what do alpha-tubulin and beta-tubulin do

A

form tubulin dimers which repeat over and over in a coil, forming a long tube

85
Q

what are vinca alkaloids

A

bind to tubulin dimers and inhibit them from joining a microtubule

86
Q

with vinca-alkaloids, the dimer-alkaloid complexes do what

A

form crystals which can cause damage to cell parts

87
Q

5 most common vinca alkaloids

A

vincristine, vinblastine, vindesine, vinorelbine, vinflurine

88
Q

vinca alkaloids names

A

vin-

89
Q

failure of the mitotic spindle + extra damage will lead too

A

activation of p53

90
Q

to function correctly in spindles…. microtubules must

A

undergo polymerization

undergo depolymerization

91
Q

polymerization

A

building up

92
Q

depolymerization

A

being broken down again

93
Q

the spindle only works when

A

when microtubules are broken apart, pulling pieces towards an end

94
Q

taxanes

A

class of drug that bind to fully formed microtubules and inhibit depolymerization

95
Q

wif the microtubules do not to depolymerization

A

the spindle does not operate»> p53»> death

96
Q

taxanes usually end in

A

taxel

97
Q

what impede the mitotic spindle from forming

A

taxanes

98
Q

anthracyclines orginated from what

A

streptomyces peucetius… a species of soil dwelling bacteria

99
Q

vinca alkaloids were originally derived from

A

species of periwinkle found in madagascar

100
Q

taxanes were first discovered where

A

in the bark of yew tree

pathophysiology (24 decks)

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