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Foundations of Medicine > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

<p>What are treatment options for cancer?</p>

A

<p>Surgery</p>

<p>Radiotherapy</p>

<p>Chemotherapy</p>

<p>Targeted therapies</p>

<p>Immunotherapy</p>

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2
Q

<p>What are the steps of the cell cycle?</p>

A

<p>G1 (gap 1, preparation for DNA replication)</p>

<p>R (restriction point, point in G1 where the cell becomes committed)</p>

<p>S (DNA replication)</p>

<p>G2 (preparation for mitosis)</p>

<p>M (mitosis, cell divsion)</p>

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3
Q

<p>What happens during G1 (gap 1)?</p>

A

<p>Preparation for DNA replication</p>

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4
Q

<p>What is R during the cell cycle?</p>

A

<p>Restriction point, where the cell become committed</p>

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5
Q

<p>What happens during S?</p>

A

<p>DNA replication</p>

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6
Q

<p>What happens during G2?</p>

A

<p>Preparation for mitosis</p>

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7
Q

<p>What happens during M?</p>

A

<p>Mitosis, cell division</p>

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8
Q

<p>What are things that make the cell cycle go around?</p>

A

<p>Growth factors</p>

<p>Oncogenes</p>

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9
Q

<p>What makes the cell cycle stop?</p>

A

<p>Tumour suppresor genes</p>

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10
Q

<p>What does chemo delivery do?</p>

A

<p>Reduces the amount of cells</p>

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11
Q

<p>What happens if the interval between chemo delivery is to long?</p>

A

<p>The cells grow back</p>

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12
Q

<p>How is systematic therapy delivered?</p>

A

<p>Oral or intravenous route</p>

<p>Regular cycles with timing dependent on the findings from pharmacokinetics (half life, excretion)</p>

<p>May need to delay treatment if toxicites develop</p>

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13
Q

<p>What needs to happen to chemotherapy if toxicities develop?</p>

A

<p>It needs to be delayed</p>

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14
Q

<p>What are methods of assessing drug therapy?</p>

A

<p>CT scan</p>

<p>PET scan</p>

<p>Clinical examination</p>

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15
Q

<p>What may assessing drug activity help?</p>

A

<p>Overall survival (OS)</p>

<p>Progression-free survival (PFS)</p>

<p>Improved quality of life (QoL)</p>

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16
Q

<p>What is progression free survival?</p>

A

<p>Length of time during and after treatment of a disease that a patient lives with the disease but it does not get any worse</p>

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17
Q

<p>What is overall survival?</p>

A

<p>The length of time from either the diagnosis or the start of treatment for a disease that the patient is still alive</p>

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18
Q

<p>What does an adjuvant do?</p>

A

<p>Improve survival</p>

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19
Q

<p>What does a neoadjuvant do?</p>

A

<p>May improve survival through increasing operability</p>

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20
Q

<p>What is adjuvant treatment?</p>

A

<p>Treatment given in addition to a primary treatment</p>

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21
Q

<p>What is neoadjuvant chemotherapy?</p>

A

<p>Medicines administered before surgery for the treatment of cancer</p>

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22
Q

<p>What are some different classes of cytotoxic agents?</p>

A

<p>Alkylating agents</p>

<p>Anti-metabolites</p>

<p>Mitotic inhibitors</p>

<p>Antibiotics</p>

<p>Other</p>

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23
Q

<p>What are some sites of action for cytotoxic agents?</p>

A

<p>Anti-metabolites prevent RNA synthesis by binding to DNA</p>

<p>Alkylating agents cross link guanine nucleobases, directly attacking DNA</p>

<p>Intercalating agents wedge between bases along DNA to stop polymerase and other proteins from binding (preventing DNA transcription and DNA duplication)</p>

<p>Spindle poisons act on tubulin, which forms the microtubules that attach to chromosomes during mitosis</p>

24
Q

<p>What do alkylating agents do?</p>

A

<p>Attach to free guanines on seperated DNA strands, impairing DNA replication</p>

25
Q

<p>What does the alkyl group of an alkylating agent allow?</p>

A

<p>Covalent bonds with other molecules</p>

26
Q

<p>What is an example of an alkylating agent?</p>

A

<p>Cisplatin</p>

27
Q

<p>What are some mechanisms of resistance against alkylating agents?</p>

A

<p>Decreases entry or increases exit of agent in cell</p>

<p>Inactivation of agent in cell</p>

<p>Enhanced repair of DNA lesions produced by alkylation</p>

28
Q

<p>How do antimetabolites work?</p>

A

<p>Similar structure to essential metabolites required by cell prior to cell division</p>

<p>Can be incorporated into new nuclear material or bind with vital enzymes</p>

29
Q

<p>What are examples of antimetabolites?</p>

A

<p>Antagonise folic acid</p>

<p>Antagonis purine</p>

30
Q

<p>What are examples of spindle poisons?</p>

A

<p>Vinca alkaloids</p>

<p>Taxanes</p>

31
Q

<p>What do vinca alkaloids do?</p>

A

<p>Metaphase arrest agents, blocking microtubule formation and spindle formation</p>

32
Q

<p>What do taxanes do?</p>

A

<p>Promote spindles and freeze cells at that stage</p>

33
Q

<p>What are the 2 classes of antimiotic antibiotics?</p>

A

<p>Anthracyclines</p>

<p>Non-anathracyclines</p>

34
Q

<p>What do antimiotic antibiotics do?</p>

A

<p>Intercalate and inhibit DNA and RNA synthesis</p>

<p>Bind to membranes and increase permeability of ions</p>

<p>Free radicals disrupt DNA chain and prevent mitosis</p>

35
Q

<p>Where during the cell cycle do alkylating agents act?</p>

A

<p>All of the stages</p>

36
Q

<p>Where during the cell cycle do antibiotics act?</p>

A

<p>End of G1 through to the start of G2</p>

37
Q

<p>Where during the cell cycle do antimetabolites?</p>

38
Q

<p>Where during the cell cycle do metabolic inhibitors act?</p>

A

<p>During M</p>

39
Q

<p>What is the aim of combination therapy?</p>

A

<p>Increase efficacy</p>

40
Q

<p>What are the principles underlying combination therapy?</p>

A

<p>Different mechanisms of action</p>

<p>Dissimilar toxicity profile (such as both do not act with neurotoxicity)</p>

41
Q

<p>What does having different mechanisms of action during combination therapy allow?</p>

A

<p>Synergistic or at least additive</p>

<p>Reduce risk of developing resistance</p>

42
Q

<p>What are some possible side effects of chemotherapy?</p>

A

<p>Vomiting</p>

<p>Nausea</p>

<p>Alopecia (loss of hair)</p>

<p>Tiredness</p>

43
Q

<p>What does moderately emetogenic chemotherapy refer to?</p>

A

<p>Moderate incidences of nausea and vomiting</p>

44
Q

<p>What does highly emetogenic chemotherapy refer to?</p>

A

<p>High incidents of nausea and vomiting</p>

45
Q

<p>What is CINV?</p>

A

<p>Chemotherapy induced nausea and vomiting</p>

46
Q

<p>What is peripheral CINV?</p>

A

<p>Where drugs act on enterochromaffin cells in the gastric glands which release serotonin which acts on vagal afferent 5-HT3 receptors</p>

47
Q

<p>Where do the gastric glands release during peripheral CINV?</p>

A

<p>Serotonin</p>

48
Q

<p>What does serotonin act on during peripheral CINV?</p>

A

<p>5-HT3receptors</p>

49
Q

<p>What is central CINV?</p>

A

<p>Drugs act on brainstem NK3receptors and cause CINV</p>

50
Q

<p>What are examples of hormonal drugs?</p>

A

<p>Anti-oestrogen for breast cancer</p>

<p>Gonadorelin analogue</p>

<p>Anti-adrogen for prostate cancer</p>

51
Q

<p>What is anti-oestrogen used for?</p>

A

<p>Breast cancer</p>

52
Q

<p>What is anti-adrogen used for?</p>

A

<p>Prostate cancer</p>

53
Q

<p>What are some things targeted drugs act against?</p>

A

<p>Epidermal growth factor receptor (EGFR)</p>

<p>Vascular endothelial growth receptor (VEGR)</p>

54
Q

<p>What receptors do T lymphocytes have?</p>

A

<p>Activation and inhibitory receptors</p>

55
Q

<p>How does immunotherapy work?</p>

A

<p>Cancer cells hide from the immune system by binding to the self receptor PD1, but drugs can inhibit this</p>

Foundations of Medicine (167 decks)

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