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Genetics and Neoplasia > GN Cancer Chemotherapies and Flipped Classroom > Flashcards

GN Cancer Chemotherapies and Flipped Classroom Flashcards

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1
Q

What is pharmacodynamics?

A

How drugs affect the body

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2
Q

How are the vinca drugs excreted?

A

Biliary excretion

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3
Q

Why are alkylating not a preferential treatment in pediatrics patients?

A

There many secondary malignancies that arise as a result of alkylating agent chemo. (This concern is inversely proportional to age of patient)

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4
Q

What are the acute adverse effects of mechlorethamine?

A

Nausea, vomiting

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5
Q

Are alkylating agents CCNS or CCS? What type of cells are more sensitive to alkylating agents?

A

CCNS; replicating cells

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6
Q

Cardiotoxicity is the signature adverse effect of what drug?

A

Anthracyclines: doxorubicin and daunorubicin

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7
Q

Topo I in inhibited by what drug?

A

Irinotecan

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8
Q

What does 5-FU inhibit? What required to aid in this inhibition?

A

Thymidylate synthase; enhanced by leucovorin (folinic acid) - inactivation requires both 5-FU and folinic acid

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9
Q

How can methotrexate be administered?

A

Orally, IV, or intrathecally

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10
Q

How is cis-platin administered? and cleared?

A

Intravenous, cleared in urine

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11
Q

Most alkylating agents are bifunctional. What is meant by bifunctional?

A

They are able to bind and cross-link adjacent bases or they can bind and cross-link bases on opposite strands

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12
Q

What inactivates SN-38 (the active metabolite of irinotecan)?

A

Glucouronidation by UGT1A1

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13
Q

How have STIs (single transduction inhibitors) transformed cancer?

A

From “curable” disease to a “manageable” disease

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14
Q

What drug blocks growth factor signaling in chronic myelogenous leukemia (CML)?

(Buzz association: CML = philadelphia chromosome)

A

Imatinib (inhibits Bcr-Abl and other tyr kinases)

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15
Q

When would an alkylating agent be ill-advised?

A

If the a cell has a p53 mutation (like Li Fraumeni), then inducing DNA damage wouldn’t result in apoptosis which is the desired effect.

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16
Q

What are 3 ways to classify drugs?

A

Chemical structure, mechanism of action, and therapeutic use

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17
Q

What are the four branches of pharmacology?

A

pharmacokinetics, pharmacodynamics, adverse effects, and pharmaacotherapeutics

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18
Q

What might cause a patient have a fatal myelosuppression incident when administered a standard dose of 6-mercaptopurine?

A

A defect in one or both TMPT

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19
Q

Though alkylating agents and antitumor antibiotics are CCNS what are they most effective against?

A

Rapidly proliferating cells

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20
Q

What is used as a “rescue” to prevent the cytotoxicity of methotrexate to normal cells?

A

Leucovorin (folinic acid)

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21
Q

Patient is given FOLFIRI which is made up of 5-FU, Leucovorin, and Irinotecan. The patient is genotyped and found to be UGT1A1*3*7. What would be the appropriate response to this genotype?

A

Decreasing irinotecan dosing to decrease the amount of toxic metabolites

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22
Q

What does gefitinib inhibit?

A

EGF-R tyr kinase

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23
Q

What drug is a cytosine analog and inhibits polymerase and is a chain terminator?

A

Gemcitabine

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24
Q

How are doxorubicin and daunorubicin administered?

A

intravenous, metabolized in liver

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25
Q

What causes the cystitis that results from cyclophosphamide? What drug can be administered to almeloriate these effects?

A

Acrolein; Mesna

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26
Q

Which isomerase does irinotecan inhibit?

A

Topo I

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27
Q

To which class do doxorubicin daunorubicin belong?

A

Antitumor antibiotics: anthracyclines; block Topo II

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28
Q

What specific cancer is gefitinib indicated for? What are some factors that can better the outcome?

A

Non-small cell lung cancer; better when pt is an Asian non-smoking woman

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29
Q

45 year old female pt will be treated with a combination of Doxorubicin, docetaxel, and cyclophosphamide. Desrazoxane may be added in order to?

A

Protect against doxorubicin cardiotoxicity. Doxorubicin generates free radicals and desrazoxane acts as a free radical scavenger.

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30
Q

sterile hemorrhagic cystitis is the hallmark side effect of what?

A

Cyclophosphamide

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31
Q

What is the key adverse effect of bleomycin?

A

Pulmonary fibrosis

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32
Q

What three events stop STI treatments?

A

Tumor gains resistance, patient dies, patients choose to discontinue the drug (this shit ain’t cheap)

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33
Q

What are two ways that resistance can be mounted to 6-MP and 6-TG?

A

Decreased hprt activity (the activating step) or an increase in alkaline phosphotase

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34
Q

What is the key target of alkylating agents?

A

DNA

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35
Q

What is the class of drugs do the vinca drugs belong to? How do they work?

A

MT poison; inhibit/reverses tubulin polymerization leading to metaphase arrest (destabilizing)

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36
Q

Why is MDR-1 important in drug resistance?

A

MDR-1 uses ATP to actively transport drug out of the cell. It can also export multiple classes of anti-cancer drugs (antimetabolites, antibiotics, alkaloids, etc.)

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37
Q

When would trastuzumab not be beneficial despite the cancer being Her2/neu positive?

A

In brain metastases (monoclonal ab’s cannot cross the BBB)

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38
Q

Irinotecan is administered as a prodrug, what converts it into the active SN-38 form?

A

Esterase

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39
Q

What is the mechanism of cis-platin?

A

It is a bifunctional “platinating agent” that cross-links DNA

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40
Q

What type of drug is Tamoxifen?

A

Selective estrogen receptor antagonists (SERMs), competing ligands for ER (ER antagonist in breast)

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41
Q

What are some resistance mechanisms to alkylating agents?

A

Impermeable to drug, pump drug out (MDR), or alternate targets for drug (glutathione), increased DNA repair, Lack of apoptosis

42
Q

What is the dose-limiting toxic effect of alkylating agents?

A

Decreased leukocytes and platelets

43
Q

How are the Taxanes different than the Vincas?

A

These drugs result in stabilization of the MTs and block progress through mitosis

44
Q

What type of analog is methotrexate? How does it work?

A

Folate; It acts as a dihydrofolate reductase (DHFR) substrate and inhibitor. Thus, limiting folic acid that typically acts the carbon carrier when you want to add one carbon. Most importantly, blocking the formation of thymidine

45
Q

What are the taxane drugs?

A

Paclitaxel and Docetaxel

46
Q

Although cyclophosphamide is classed as cell-cycle non-specific, is it still more effective against proliferating cells. Why is this?

A

This minimizes the time for DNA repair to occur

47
Q

If a patient becomes resistant to imatinib, what can given to overcome this resistance?

A

Dasatinib (2nd gen Bcr-Abl inhibitor)

48
Q

What drug acts as a monoclonal antibody against Her2/neu oncogene product?

A

Trastuzumab

49
Q

Vinblastine will have what side effect that wont be as sever in Vincristine?

A

Bone marrow suppression

50
Q

Renal toxicity is the hallmark side effect of what alkylating agent

A

Cis-platin

51
Q

What is Bleomycin?

A

It is an antitumor antibiotic, mixture of glycopeptides

52
Q

Vinca drugs cause what?

A

Metaphase arrest

53
Q

What CCNS drug is most effective in the G2 stage?

A

Bleomycin

54
Q

Since rapidly growing cells are most effected by alkylating agents, what sites are most effected in the body?

A

BM, GI tract, spermatogenesis

55
Q

What are two aromatase inhibitors? What types of breast cancer are they indicated for?

A

Anastrazole, Letrozole; treatment for ER+ primary and metastatic breast cancers

56
Q

What alkylating agent is inject in a prodrug form that will be metabolized by the host’s liver?

A

Cyclophosphamide

57
Q

What is the half-life of mechlorethamine?

A

Several minutes. The drug was be administered rapidly because of this.

58
Q

Imatinib and Dasatinib are what type of drugs?

A

Tyrosine kinase inhibitors

59
Q

How can cyclophosphamide be administered?

A

Oral or intravenous

60
Q

Which drugs are the anthracyclines that block topo II?

A

Doxorubicin and daunorubicin

61
Q

What are the adverse effects of cyclophosphamide?

A

Nausea, vomiting, alopecia, sterile hemorrhagic cystitis (signature adverse effect)

62
Q

What does imatinib inhibit?

A

Inhibits BCR-ABL and also blocks growth factors associated with CML.

63
Q

How do the side effects of aromatase inhibitors compare to chemotherapy side effects?

A

They are way more mild, symptoms are similar to menopause

64
Q

What are the side effects of Vincristine?

A

Peripheral neuropathy. Ideal because of no bone marrow depression

65
Q

What is an antimetabolite?

A

An analog of a normal component in the target cell, which will compete with the normal component. Ultimately, it can block or alter that pathway.

66
Q

What is the important enzyme that metabolizes Taxomifen?

A

CYP2D6

67
Q

In the drug combination FOLFIRI is made up of 5-FU, Leucovorin, and irinotecan. Which of these drugs is activated by an esterase?

A

Irintotecan - Activated by carboxylesterase enzymes

68
Q

What is synergism and its use in chemotherapy?

A

The total effect of the combination is greater than the sum of its parts. It allows for lower doses of the individual drug minimizing toxicity and resistance to the drug

69
Q

What is the importance of Dasatinib?

A

This is a second generation BCR-ABL inhibitor, and overcame some of the Imatinib resistance

70
Q

Delivery of paclitaxel in cremophor can result in what?

A

It can result in a hypersensitivity reaction

71
Q

What is the key activating metabolizer of tamoxifen?

A

CYP2D6

72
Q

What is Gemcitabine? What is its mechanism?

A

Cytosine analog, inhibits polymerase and chain terminator

73
Q

Gefitinib does what?

A

Inhibits EGF-R tyrosine kinase.

74
Q

Anastrazole and letrozole are what?

A

Aromatase inhibitors

75
Q

Is toxicity to pathogen vs. host relative or absolute?

A

Most often it’s relative, there are many factors that can influence toxicity

76
Q

In the drug combination FOLFIRI is made up of 5-FU, Leucovorin, and irinotecan. What is the purpose of leucovorin?

A

It maximizes thymidylate synthase inactivation and provides the reduced folate helping the performance of 5-FU

77
Q

What are the two pyrimidine analogs? How does their toxicity compare to the purine analogs?

A

5-fluorouracil and Gemcitabine; Far more toxic (GI, BM)

78
Q

What are some antineoplastic targets?

A

Synthesis of bases, the conversion of ribose nucleotides to deoxyribose nucleotides, block RNA and DNA txn, Bind DNA directly

79
Q

What percentage of chemotherapeutic agents are toxic?

A

All

80
Q

Hormonal require what to be effacious?

A

Functional hormone receptor

81
Q

Active hprt pathway is required for which drugs to work?

A

6-mercaptopurine and 6-thioguanine

82
Q

What class of drug is flutamide?

A

Androgen receptor antgonist (non-steriodal ligand for AR, diminished androgen effects)

83
Q

What alkylating agents is injected only intravenously in an active form that is caustic to the skin? What is it molecular composition?

A

Mechlorethamine, nitrogen mustard

84
Q

What is used to inactivate and clear purine analongs?

A

Thiopurine methyltransferase (TPMT)

85
Q

What is the signature adverse effect of anthracyclines (doxorubicin and daunorubicin)? What drug is used to counteract this effect?

A

Cardiotoxicity (the anthracyclines concentrate in the mitochondria of cardiomyocytes causing them to burst. Killing the energy source of the cardiomyocytes); Dexrazoxane

86
Q

How does the mechanism of 6-mercaptopurine and 6-thioguanine differ?

A

6-MP inhibits synthesis of AMP and GMP

6-TG gets incorporated into RNA and DNA altering function

87
Q

What drugs act as tyrosine kinase inhibitors?

A

Imatinib, dasatinib, and gefitinib (-inibs)

88
Q

When striving for toxicity, what is the ideal type of toxicity? Define it.

A

Selective toxicity: targeting the pathogen (in this case, tumor) rather host

89
Q

Once doxorubicin and daunorubicin intercalate into DNA and block Topo II, what do they generate?

A

Free Radicals

90
Q

How can cells become resistant to methotrexate?

A

Decreased drug accumulation, amplified DHFR, altered DHFR

91
Q

What is special about the delivery of taxane drugs?

A

They have to be administered in cremophor or nanoparticles

92
Q

What are the three classes of analogs of anticancer antimetabolites?

A

Folate, purine, pyrimidine

93
Q

What are the two purine analogs? What do they require to become activated?

A

6-mercaptopurine and 6-thioguanine; purine salvage pathway (hprt) - this takes these purine analogs and adds a ribose phosphate

94
Q

Most antitumor antibodies are CCNS, bleomycin is an exception to that. What cell cycle stage is bleomycin specific to?

A

G2

95
Q

Following resection of stage 3 NSCLC, adjuvant chemotherapy is prescribed. The drugs chosen are cis-platin, paclitaxel, methotrexate and leucovorin. Why is leucovorin included?

A

Leucovorin is thought to minimize the effects of methotrexate on normal cells.

96
Q

What is the mechanism of action of alkylating agents?

A

Covalently bind to/modify biological molecules

97
Q

Following resection of stage 3 NSCLC, adjuvant chemotherapy is prescribed. The drugs chosen are cis-platin, paclitaxel, methotrexate and leucovorin. If renal toxicity is to be minimized, the patient should do what?

A

Be aggressively hydrated prior to treatment

98
Q

What drug acts as a dihydrofolate reductase substrate inhibitor blocking the formation of thymidine?

A

Methotrexate

99
Q

What is pharmacokinetics?

A

How the body affects drugs

100
Q

SN-38 (the active metabolite of irinotecan) is known to be toxic to bone marrow and GI intestinals cells (dose-limiting diarrhea). A mutant form of UGT1A1 would have what effect on dosing?

A

Mutants are typically less effective. Since UGT1A1 is protective against the diarrhea, a mutant UGT1A1 would likely reduce the tolerable dosage of that individual

101
Q

What is the signature adverse effect of cis-platin? How can it be limited?

A

Renal Toxicity; overhydrate patients before administering the cis-platin

Genetics and Neoplasia (35 decks)

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