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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
Give an example of a cancer with a high growth fraction
Burkett's lymphoma
26
What is the growth fraction in Burkett's lymphoma?
50% (doubling time of 24 hours)
27
Give an example of a cancer with a low growth fraction?
Some adenocarcinomas
28
What is the growth fraction in some adenocarcinomas?
Immeasurable (doubling time of up to 200 days)
29
What can chemotherapy agents be divided into?
- Cell cycle independent | - Cell cycle dependent
30
What can chemotherapy agents that are cell cycle dependent be further subdivided into?
- Phase non-specific | - Phase specific
31
What is meant by a chemotherapy agent being phase non-specific?
They are equally active against cells in all phases of the cell cycle except G0
32
What is meant by a chemotherapy agent being phase specific?
It is only active against cells in one phase of the cycle
33
How can if a chemotherapy is phase specific or phase non-specific be utilised clinically?
These features can be used to design drug regimen combinations and schedules that take advantage of individual drug characteristics
34
Where kind of cells does the normal process of tissue renewal involve?
Both actively proliferating and quiescent stem cells
35
What is true of the quiescent stem cells that are involved in normal tissue renewal?
They are in the G0 phase of the cell cycle
36
Why is it significant that quiescent stem cells involved in normal tissue renewal are in the G0 phase of the cell cycle?
Because most anti-cancer agents are not active against these cells
37
What is a single clonogenic malignant cell capable of?
Multiplying and ultimately killing the host
38
What does the fact that a single clonogenic malignant cell is capable of multiplying and ultimately killing the host imply?
That cure depends on total cell eradication of all malignant cells
39
Is it always the case that cure depends on total cell eradication in cancer?
No
40
Why is it not the always case that cure depends on total cell eradication of all malignant cells?
There is evidence that in some cancers, there is a host response that may augment chemotherapeutic cancer kill
41
What is the simplest model of tumour growth?
Exponential
42
When is the exponential model of tumour growth true?
Only for microscopic lesions with fewer than 10^9 tumour cells
43
What does the growth curve of a clinically palpable cancer follow?
A Gompertzian function
44
What is a Gompertzian function?
When the rate of growth slows as the tumour increases in size
45
Why does the rate of growth of a tumour slow as it increases in size?
Due to limits imposed by the tumour micro-environment
46
What is the result of larger volume cancers having smaller growth fractions?
They may be inherently less sensitive to phase-specific agents
47
What is the rationale for adjuvant chemotherapy?
Small or micrometases may be more sensitive to chemotherapy
48
What is the dose response for most chemotherapies?
Steep dose response
49
What is meant by a steep dose response to chemotherapy?
There is a greater cell kill demonstrated at higher drug doses
50
Other than dose, what other factors might influence cell kill?
- Dose intensity | - Density
51
Is resistance to chemotherapy innate or acquired during treatment?
Can be either
52
What features make it more likely that drug-resistance cells will be present?
- Larger tumour mass | - Moe doublings occurring before treatment
53
When can multi-drug resistance be observed in cancer cells?
After exposure to a single drug
54
What are cancer cells that are multi-drug resistant after being exposed to a single drug usually susceptible to?
- Alkylating agents | - Anti-metabolites
55
What is multi-drug resistance associated with?
Increased expression of the membrane protein p-glycoprotein
56
What is the function of p-glycoprotein?
Functions as an active pump transporting toxic alkaloids out of the cell
57
How is the risk of resistance to chemotherapy minimised?
Anti-cancer drugs are often combined
58
What are the different classes of chemotherapy?
- Alkylating agents - Intercalating agents - Topisomerase I/II inhibitors - Antimetabolites - Tubulin binders
59
What can alkylating agents be subdivided into?
- Bifunctional alkylating agents | - Monofunctional alkylating agents
60
Give an example of a bifunctional alkylating agent
Cyclophosphamide
61
Give an example of a monofunctional alkylating agent
Dacarbazine
62
How do bifunctional alkylating agents work?
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
What are the purine bases of DNA?
- Adenine | - Guanine
64
What is the result of bifunctional alkylating agents acting by inhibiting DNA synthesis?
They act during the S phase of the cell cycle
65
Can bifunctional alkylating agents act on more than one base?
Yes
66
Are bifunctional alkylating agents more or less cytotoxic than monofunctional alkylating agents?
More
67
How do monofunctional alkylating agents work?
They cannot form cross-links, but form adducts. This inhibits DNA synthesis
68
What is the result of monofunctional alkylating agents acting by inhibiting DNA synthesis?
They act during the S phase of the cell cycle
69
What is the disadvantage of monofunctional alkylating agents compared to bifunctional?
They are more mutagenic and carcinogenic than bifunctional
70
What can intercalating agents be subdivided into?
- Platinum compounds - Anthracyclines - Anthraquinones
71
Give 3 examples of platinum compounds?
- Cisplatin - Carboplatin - Oxaliplatin
72
How do platinum compounds act as chemotherapy agents?
They intercalate and disrupt the steric integrity of the DNA double helix, but also form intrastrand adducts like those formed by alkylating agents
73
Give 3 examples of anthracyclines
- Doxorubicin - Danorubicin - Epirubicin
74
How do anthracyclines work?
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
Is anthracyclines action base specific?
No
76
Why is anthracyclines action not base specific?
Because it's action is non-covalent
77
What is the main target for anthracyclines?
The enzyme topoisomerase II
78
Give an example of a topoisomerase I inhibitor
Topetecan
79
Give an example of a topoisomerase II inhibitor?
Etoposide
80
What do topoisomerase enzymes do?
Prevent DNA strands from becoming tangled
81
How do topoisomerase enzymes prevent DNA strands from becoming tangled?
By cutting DNA and allowing it to wind or unwind
82
What does topoisomerase I do?
Breaks single-stranded DNA and relieves torsion
83
In what phase of the cell cycle to topoisomerase I inhibitors act?
S phase
84
What do topoisomerase I inhibitors do?
They precent the re-ligation step of the nicking-closing reaction, trapping topoisomerase I in a covalent complex with the DNA
85
What does topoisomerase II do?
It breaks both strands of DNA, and allows the other strange to pass through the re-ligate
86
What do topoisomerase II inhibitors cause?
Double-stranded DNA breaks
87
What can anti-metabolites be divided into?
- Anti-folates - Pyrimidine analogues - Purine analogues
88
What are antimetabolites structurally related to?
Natural compounds
89
What do antimetabolites do?
Inhibit the metabolism of compounds necessary for DNA, RNA, or protein synthesis
90
When in the cell cycle are most anti-metabolites active?
During the S phase
91
Give two examples of anti-folates
- Methotrexate | - Ralitrexed
92
Give 3 examples of pyramidine analogues
- 5-FU - Gemcitabine - Cytosine arabinoside
93
Give 2 examples of purine analogues
- 6-metacaptopurine | - 6-thioguanine
94
What can tubulin binders be subdivided into?
- Vinca alkaloids | - Taxanes
95
Give 2 examples of vinca alkaloids
- Vincristine | - Vinblastine
96
How do vinca alkaloids work?
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
Give 2 examples of taxanes
- Paclitaxel | - Docetaxel

Z - Cancer Care Old (28 decks)

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