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X - Cancer Care COPY > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

What does chemotherapy involve?

A

The use of pharmacological agents to kill tumour cells

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2
Q

What can chemotherapy be effective in treating?

A

Both primary tumours and metastatic spread

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3
Q

How does chemotherapy work?

A

It acts at different stages of the cell cycle, and exerts its effects primary by 3 different mechanisms;

  • Altering the chemistry of nucleic acids
  • Interfering with DNA or RNA synthesis
  • Disrupting mechanisms of cell devision
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4
Q

Are chemotherapy agents selective?

A

Most of the common agents act in a non-selective manner

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5
Q

What is meant by most chemotherapy agents acting in a non-selective manner?

A

They not only damage cancer cells, but affect normal dividing cells

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6
Q

What normal dividing cells are particularly affected by chemotherapy?

A
  • Hair follicles
  • Bone marrow
  • Gastrointestinal mucosa
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7
Q

What is the result of chemotherapy agents acting in a non-selective manner?

A

It produces side effects that limit the dose that can be administered and the recovery time before the next dose can be given

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8
Q

How is most chemotherapy given?

A

As a combination of drugs administered IV on an intermittent basis

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9
Q

On average, how often is an individual cycle of chemotherapy repeated?

A

Every 21-28 days

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10
Q

How many cycles does a typical course of chemotherapy consist of?

A

6

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11
Q

What is the purpose of intermittent dosing in chemotherapy?

A

Malignant cells have less capacity for repair than normal cells, and intermittent dosing exploits the fact that tumour cells recover from cytotoxic damage more slowly than normal cell populations

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12
Q

What does each sequential treatment cycle of chemotherapy allow?

A

Normal stems cells time to recover

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13
Q

What is the chemotherapy drug dose usually calculated from?

A

Surface area of patient, based on height and weight

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14
Q

What is pharmacodynamics?

A

The study of the effect that drugs have in the body

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15
Q

Why is pharmacodynamics significant in chemotherapy?

A

In terms of dose-limiting toxicity, which can be used to determine the maximum possible dose in an individual patient

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16
Q

What is pharmacokinetics?

A

The study of the effects that the body has on the drug

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17
Q

What can pharmacokinetics be modified by?

A
  • Renal and hepatic function

- Drugs clearance from the circulation

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18
Q

What is the result of the potential for modification of pharmacokinetics with chemotherapy?

A

Careful monitoring of the patient’s biochemistry, renal, liver, and bone marrow function is essential during chemotherapy treatment

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19
Q

What is the downside of chemotherapy?

A

It is highly toxic with the potential for life-threatening side effects

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20
Q

How is the potential for life threatening side effects of chemotherapy reduced?

A
  • Requires supervision from specialists

- Patients should have careful assessment prior to commencement of treatment, and prior to each cycle

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21
Q

What is a reliable predictor to tolerance of chemotherapy treatment?

A

Patient fitness

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22
Q

What is the result of poor fitness when having chemotherapy?

A
  • Will not tolerate chemotherapy as well

- Increased risk of adverse effects

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23
Q

How is the effects of poor fitness in chemotherapy patients combatted?

A

It is important to assess the patient’s performance status to determine patient suitability for chemotherapy and appropriate dosing of treatments

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24
Q

What is growth fraction?

A

The percentage of cells in a tumour mass that are actively dividing

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25
Q

Give an example of a cancer with a high growth fraction

A

Burkett’s lymphoma

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26
Q

What is the growth fraction in Burkett’s lymphoma?

A

50% (doubling time of 24 hours)

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27
Q

Give an example of a cancer with a low growth fraction?

A

Some adenocarcinomas

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28
Q

What is the growth fraction in some adenocarcinomas?

A

Immeasurable (doubling time of up to 200 days)

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29
Q

What can chemotherapy agents be divided into?

A
  • Cell cycle independent

- Cell cycle dependent

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30
Q

What can chemotherapy agents that are cell cycle dependent be further subdivided into?

A
  • Phase non-specific

- Phase specific

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31
Q

What is meant by a chemotherapy agent being phase non-specific?

A

They are equally active against cells in all phases of the cell cycle except G0

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32
Q

What is meant by a chemotherapy agent being phase specific?

A

It is only active against cells in one phase of the cycle

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33
Q

How can if a chemotherapy is phase specific or phase non-specific be utilised clinically?

A

These features can be used to design drug regimen combinations and schedules that take advantage of individual drug characteristics

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34
Q

Where kind of cells does the normal process of tissue renewal involve?

A

Both actively proliferating and quiescent stem cells

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35
Q

What is true of the quiescent stem cells that are involved in normal tissue renewal?

A

They are in the G0 phase of the cell cycle

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36
Q

Why is it significant that quiescent stem cells involved in normal tissue renewal are in the G0 phase of the cell cycle?

A

Because most anti-cancer agents are not active against these cells

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37
Q

What is a single clonogenic malignant cell capable of?

A

Multiplying and ultimately killing the host

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38
Q

What does the fact that a single clonogenic malignant cell is capable of multiplying and ultimately killing the host imply?

A

That cure depends on total cell eradication of all malignant cells

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39
Q

Is it always the case that cure depends on total cell eradication in cancer?

A

No

40
Q

Why is it not the always case that cure depends on total cell eradication of all malignant cells?

A

There is evidence that in some cancers, there is a host response that may augment chemotherapeutic cancer kill

41
Q

What is the simplest model of tumour growth?

A

Exponential

42
Q

When is the exponential model of tumour growth true?

A

Only for microscopic lesions with fewer than 10^9 tumour cells

43
Q

What does the growth curve of a clinically palpable cancer follow?

A

A Gompertzian function

44
Q

What is a Gompertzian function?

A

When the rate of growth slows as the tumour increases in size

45
Q

Why does the rate of growth of a tumour slow as it increases in size?

A

Due to limits imposed by the tumour micro-environment

46
Q

What is the result of larger volume cancers having smaller growth fractions?

A

They may be inherently less sensitive to phase-specific agents

47
Q

What is the rationale for adjuvant chemotherapy?

A

Small or micrometases may be more sensitive to chemotherapy

48
Q

What is the dose response for most chemotherapies?

A

Steep dose response

49
Q

What is meant by a steep dose response to chemotherapy?

A

There is a greater cell kill demonstrated at higher drug doses

50
Q

Other than dose, what other factors might influence cell kill?

A
  • Dose intensity

- Density

51
Q

Is resistance to chemotherapy innate or acquired during treatment?

A

Can be either

52
Q

What features make it more likely that drug-resistance cells will be present?

A
  • Larger tumour mass

- Moe doublings occurring before treatment

53
Q

When can multi-drug resistance be observed in cancer cells?

A

After exposure to a single drug

54
Q

What are cancer cells that are multi-drug resistant after being exposed to a single drug usually susceptible to?

A
  • Alkylating agents

- Anti-metabolites

55
Q

What is multi-drug resistance associated with?

A

Increased expression of the membrane protein p-glycoprotein

56
Q

What is the function of p-glycoprotein?

A

Functions as an active pump transporting toxic alkaloids out of the cell

57
Q

How is the risk of resistance to chemotherapy minimised?

A

Anti-cancer drugs are often combined

58
Q

What are the different classes of chemotherapy?

A
  • Alkylating agents
  • Intercalating agents
  • Topisomerase I/II inhibitors
  • Antimetabolites
  • Tubulin binders
59
Q

What can alkylating agents be subdivided into?

A
  • Bifunctional alkylating agents

- Monofunctional alkylating agents

60
Q

Give an example of a bifunctional alkylating agent

A

Cyclophosphamide

61
Q

Give an example of a monofunctional alkylating agent

A

Dacarbazine

62
Q

How do bifunctional alkylating agents work?

A

By transferring an alkyl group to the purine bases of DNA, which forms covalent bonds between two different bases, resulting in interstrand or intrastrand cross links, therefore inhibiting DNA synthesis

63
Q

What are the purine bases of DNA?

A
  • Adenine

- Guanine

64
Q

What is the result of bifunctional alkylating agents acting by inhibiting DNA synthesis?

A

They act during the S phase of the cell cycle

65
Q

Can bifunctional alkylating agents act on more than one base?

A

Yes

66
Q

Are bifunctional alkylating agents more or less cytotoxic than monofunctional alkylating agents?

A

More

67
Q

How do monofunctional alkylating agents work?

A

They cannot form cross-links, but form adducts. This inhibits DNA synthesis

68
Q

What is the result of monofunctional alkylating agents acting by inhibiting DNA synthesis?

A

They act during the S phase of the cell cycle

69
Q

What is the disadvantage of monofunctional alkylating agents compared to bifunctional?

A

They are more mutagenic and carcinogenic than bifunctional

70
Q

What can intercalating agents be subdivided into?

A
  • Platinum compounds
  • Anthracyclines
  • Anthraquinones
71
Q

Give 3 examples of platinum compounds?

A
  • Cisplatin
  • Carboplatin
  • Oxaliplatin
72
Q

How do platinum compounds act as chemotherapy agents?

A

They intercalate and disrupt the steric integrity of the DNA double helix, but also form intrastrand adducts like those formed by alkylating agents

73
Q

Give 3 examples of anthracyclines

A
  • Doxorubicin
  • Danorubicin
  • Epirubicin
74
Q

How do anthracyclines work?

A

They intercalate into the DNA major groove between base pairs of the DNA double helix. This disrupts the steric integrity of the DNA helix, and blocks DNA replication

75
Q

Is anthracyclines action base specific?

A

No

76
Q

Why is anthracyclines action not base specific?

A

Because it’s action is non-covalent

77
Q

What is the main target for anthracyclines?

A

The enzyme topoisomerase II

78
Q

Give an example of a topoisomerase I inhibitor

A

Topetecan

79
Q

Give an example of a topoisomerase II inhibitor?

A

Etoposide

80
Q

What do topoisomerase enzymes do?

A

Prevent DNA strands from becoming tangled

81
Q

How do topoisomerase enzymes prevent DNA strands from becoming tangled?

A

By cutting DNA and allowing it to wind or unwind

82
Q

What does topoisomerase I do?

A

Breaks single-stranded DNA and relieves torsion

83
Q

In what phase of the cell cycle to topoisomerase I inhibitors act?

A

S phase

84
Q

What do topoisomerase I inhibitors do?

A

They precent the re-ligation step of the nicking-closing reaction, trapping topoisomerase I in a covalent complex with the DNA

85
Q

What does topoisomerase II do?

A

It breaks both strands of DNA, and allows the other strange to pass through the re-ligate

86
Q

What do topoisomerase II inhibitors cause?

A

Double-stranded DNA breaks

87
Q

What can anti-metabolites be divided into?

A
  • Anti-folates
  • Pyrimidine analogues
  • Purine analogues
88
Q

What are antimetabolites structurally related to?

A

Natural compounds

89
Q

What do antimetabolites do?

A

Inhibit the metabolism of compounds necessary for DNA, RNA, or protein synthesis

90
Q

When in the cell cycle are most anti-metabolites active?

A

During the S phase

91
Q

Give two examples of anti-folates

A
  • Methotrexate

- Ralitrexed

92
Q

Give 3 examples of pyramidine analogues

A
  • 5-FU
  • Gemcitabine
  • Cytosine arabinoside
93
Q

Give 2 examples of purine analogues

A
  • 6-metacaptopurine

- 6-thioguanine

94
Q

What can tubulin binders be subdivided into?

A
  • Vinca alkaloids

- Taxanes

95
Q

Give 2 examples of vinca alkaloids

A
  • Vincristine

- Vinblastine

96
Q

How do vinca alkaloids work?

A

By binding to the tubulin dimer and preventing the assembly of microtubule filaments, therefore interfering with the functinon of the mitotic spindles and preventing cell division during the M phase of the cell cycle

97
Q

Give 2 examples of taxanes

A
  • Paclitaxel

- Docetaxel

X - Cancer Care COPY (36 decks)

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