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Pharmacology > Anticancer Drugs > Flashcards

Anticancer Drugs Flashcards

1
Q

most important efflux pump responsible for multidrug resistance

A

p-glycoprotein aka multidrug resistant protein 1 (MDR1)

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2
Q

cell cycle specific agents

A

B-AMEC

Bleomycin 
Antimetabolites
Microtubule inhibitors
Epipodophyllotoxins
Camptothecins
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3
Q

what are the cell cycle non specific agents

A

Alkylating Agents
Platinum coordination complexes
Antitumor antibiotics (minus Bleomycin)

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4
Q

what are the antimetabolites

A

Folate analogues: Methotrexate

Purine analogues: 6-mercaptopurine and 6-thioguanine

Pyrimidine analogues: Fluoropyrimidines (5-fluorouracil and capecitabine) and Deoxycytidine analogues (cytarabine and gemcitabine)

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5
Q

what inhibits the renal excretion of methotrexate

A

CANP

Cephalosporin
Aspirin
NSAIDs
Penicillin

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6
Q

mechanism of action of methotrexate

A

catalyzed by folylpolyglutamate synthetase to MTX polyglutamate –> inhibits dihydrofolate reductase –> no THF –> needed for deoxythymidylate nucleotides and purine nucleotides

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7
Q

what drug is used in conjunction with MTX and why

A

Leucovorin, derivative of THF, to rescue normal cells from toxicity and overcome accidental drug overdose

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8
Q

adverse effects of MTX

A

a lot can be resolved with leucovorin

Myelosuppression
Pulmonary Fibrosis

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9
Q

mechanism of 6-mercaptopurine

A

converted to 6-MP ribose phosphate (or thio-inosinic acid or TIMP) by HGPRT –> inhibits phosphoribosyl pyrophosphate amidotransferase –> needed for de novo purine synthesis

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10
Q

what drugs/deficiency can make 6-mercaptopurine toxic

A
  • it is metabolized by xanthine oxidase so if given with allopurinol which inhibits the enzyme then 6-MP will reach toxic level if dose not reduced
  • also metabolized by TPMT (thiopurine methyltransferase) so if deficiency in allele, 6-MP can reach toxic levels if dose not reduced
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11
Q

mechanism of thioguanine

A

converted to nucleotide thioguanosine monophosphate (TGMP) by HGPRT

  • inhibits PRPP amidotransferase which inhibits purine synthesis
  • inhibits Guanylate kinase so can’t go from GMP to GDP
  • can be converted to TGTP and dTGTP which can be incorporated into RNA and DNA respectively
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12
Q

what can make a normal dose of thioguanine toxic

A

TPMT (thiopurine methyltransferase) deficiency hence thioguanine dose must be reduced

it is inactivated by deamination (not oxidation) so xanthine oxidase (allopurinol) does not play a role here

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13
Q

when treating adult acute leukemia, what drug is thioguanine used synergistically with

A

Cytarabine

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14
Q

first line drug for colorectal cancer

A

5-fluorouracil

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15
Q

mechanism of 5-fluorouracil

A

converted to FdUMP which forms a tertiary complex with thymidylate synthase and reduced folate (N5, N10, and methylene THF) –> inhibition of DNA synthesis

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16
Q

what potentiates the activity of 5-fluorouracil

A

increasing level of the reduced folate - N5, N10, and methylene THF

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17
Q

what can cause a normal dose of 5-fluorouracil to become toxic

A

deficiency of dihydropyrimidine dehydrogenase (DPD), the enzyme that metabolized it

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18
Q

adverse effects of 5-fluorouracil

A

hand foot syndrome (also seen in capecitabine)

19
Q

what catalyzes capecitabine

A

thymidine phosphorylase

20
Q

the enzyme thymidine phosphorylase is high in what cancers (name drug metabolized by enzyme)

A

breast and colorectal cancer

capecitabine

21
Q

mechanism of cytarabine

A

converted to cytosine arabinoside triphosphate

  • inhibits DNA pol alpha (DNA synthesis)
  • inhibits DNA pol beta (DNA repair)
  • incorporated into chain –> termination
22
Q

how is cytarabine inactivated

A

by deamination in the intestinal mucosa

23
Q

mechanism of gemcitabine

A
  • converted to gemcitabine diphosphate which inhibits ribonucleotide reductase –> reduces nucleotide needed for DNA synthesis
  • converted to gemcitabine triphosphate which incorporates into chain and causes termination
24
Q

how is gemcitabine eliminated

A

deaminated to difluorodeoxyuridine which is excreted in urine

25
Q

adverse effect of gemcitabine

A

renal microangiopathy syndromes like HUS (hemolytic uremic syndrome) and TTP (thrombotic thrombocytopenic purpura)

26
Q

what are the anticancer microtubule inhibitors and what does inhibiting microtubules do

A

Vinca Alkaloids: Vinblastine and Vincristine
Taxanes: Docetaxel and Paclitaxel

inhibits formation of mitotic spindles needed for cell division to daughter cells and also microtubules are needed for cellular functions such as movements, phagocytosis, and axonal transport

27
Q

mechanism of vinca alkaloids (name them)

A

Vinblastine and Vincristine

they bind to beta-tubulin and stops it from polymerizing with alpha-tubulin to form microtubules

28
Q

adverse of vincristine

A

Paralytic Ileus
Peripheral Neuropathy
Optic Atrophy
SIADH

29
Q

mechanism of Taxanes (name them)

A

Docetaxel and Paclitaxel

they bind to beta-tubulin (different site from vinca alkaloids) –> promote microtubule polymerization and inhibit depolymerization –> arrest cells in mitosis –> apoptosis

30
Q

condition requiring reduced dose of taxanes (name them)

A

Docetaxel and Paclitaxel

liver dysfunction

31
Q

adverse effect seen in Paclitaxel and how it is avoided

A

hypersensitivity reactions

avoided with premedication with dexamethasone, diphenhydramine, and H2 blocker

32
Q

what is Abraxane and its importance

A

albumin bound Paclitaxel formulation approved for metastatic cancer that is not associated with hypersensitivity reactions hence no need for premedication with dexamethasone, diphenhydramine, and H2 blocker

33
Q

what are the Epipodophyllotoxins

A

Etoposide

Teniposide

34
Q

mechanism of action of epipodophyllotoxins (name them)

A

Etoposide and Teniposide

inhibits topoisomerase II –> DNA damage through strand breakage

35
Q

what are the Camptothecins

A

Irinotecan

Topotecan

36
Q

mechanism of Camptothecins (name them)

A

Irinotecan and Topotecan

inhibits topoisomerase I –> needed for cutting religating single DNA strands

37
Q

what is the more potent form of Irinotecan and how are they eliminated

A

SN-38 (converted in the liver)

both eliminated in bile and feces

38
Q

adverse effects of Irinotecan

A

diarrhea with two forms

  • 1st: within 24 hours and due to cholinergic activity so stop with atropine
  • 2nd: within 2 to 10 days and can lead to electrolyte imbalance and dehydration
39
Q

what are the antitumor antibiotics

A

BADD

Bleomycin
Anthracyclines: Daunorubicin and Doxorubicin

40
Q

mechanism of bleomycin

A

binds to DNA –> free radical formation via Fe dependent process–> single and double strand breaks –> inhibition of DNA biosynthesis

41
Q

adverse effect of bleomycin

A

pulmonary fibrosis

42
Q

mechanism of anthracyclines (name them)

A

Daunorubicin and Doxorubicin

inhibits topoisomerase II

43
Q

adverse effects of anthracyclines (name them)

A

Daunorubicin and Doxorubicin

Cardiotoxicity: 2 form

  • acute: 2-3 days and is usually transient and asymptomatic
  • chronic: due to increased free radicals within the myocardium and is treated/prevented with iron chelating agent dexrazoxane

Pharmacology (79 decks)

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