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PoD topics > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

what are the possible therapeutic methods used to treat cancer? (5)

A
  1. surgery
  2. radiotherapy
  3. chemotherapy (systemic delivery/absorption, IV or oral)
  4. targeted therapies
  5. immunotherapy
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2
Q

what 3 things cause cell proliferation?

A
  1. growth factors
  2. oncogenes
  3. Cyclins and CDKs
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3
Q

what 2 things stop cell proliferation?

A
  1. tumour suppressor genes

2. CDK inhibitors

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4
Q

why does chemotherapy need to be closely administered?

A

the right line needs to be drawn between chemo administration to kill cancer and not giving too much chemo which will cause cancer

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5
Q

how is chemotherapy delivered? (2)

A
  • orally

- intravenously

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6
Q

what is the timing and regular cycles of chemotherapy dependent on?

A

Pharmacokinetics (half life, excretion)

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7
Q

why might chemotherapy cycles be delayed?

A

if toxicities develop (in bone marrow especially)

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8
Q

Chemotherapy (systemic therapy) is better for what type of tumours?

A

non-solid tumours

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9
Q

what objective methods can be used to asses drug activity? (4)

A
  1. CT scans
  2. PET scans
  3. clinical examination
  4. RECIST criteria in radiology
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10
Q

what 3 categories can “improved” method of drug activity be split into?

A
  1. overall survival
  2. progression-free survival ( time before tumour starts to grow again)
  3. improved quality of life
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11
Q

what is adjuvant treatment?

A

prevents recurrence of disease especially at distant sites, often if tumour is invasive or has unfavourable prognostic outcomes

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12
Q

what is neoadjuvant treatment?

A

administered before a surgery as drugs could possibly shrink tumour and give more surgical options

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13
Q

what are the main cytotoxic agents?

A
  1. alkylating agents
  2. anti-metabolites
  3. mitotic inhibitors
  4. antibitoics
    5 others
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14
Q

where do antimetabolites work at cellular level?

A

on DNA synthesis

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15
Q

where do alkylating agents work at cellular level?

A

on DNA directly

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16
Q

where do intercalating agents work at cellular level?

A

on DNA transcription and duplication

17
Q

where do spindle poisons /mitotic inhibitors(vinca alkaloids and taxanes) work at cellular level?

A

mitosis

18
Q

what do alkylating agents do specifically in DNA?

A
  • alkyl group allows for other covalent bods with other molecules to be made
  • attach to free guanines at N6 on separated DNA strands
  • can’t act as templates for new DNA formation
  • DNA strands linked and will not separate
  • DNA unwinding doesn’t happen because of these DNA changes (no new DNA formation, replication impaired)
19
Q

Can tumours develop resistance to alkylating agents?

A

Yes

20
Q

what are the 3 forms of resistance that tumours can develop against alkylating agents?

A
  1. Decreased entry or increased exit of agent from the cell (drug is pumped out or not allowed in)
  2. inactivation of agent in cell (glutathione deactivates drug)
  3. enhanced repair of DNA lesions produce by alkylation (enzymes repair damaged DNA)
21
Q

what do antimetabolites do on DNA synthesis?

A
  • may be incorporated to new nuclear material or bind irreversibly with vital enzymes to inhibit cell division
    e. g. methotrexate inhibit thymidylate synthase
22
Q

what does antimetabolite, methotrexate act on?

A

FH4 production which is needed for purine production. Instead 5-FU is incorporated instead of uracil in the RNA

23
Q

what does the spindle poison, vinca alkaloids do?

A
  • metaphase arrest agents

- bind to tubuli and block microtubule/spindle formation

24
Q

what does the spindle poison, taxanes do?

A

-promotes spindles and “freeze” cells at the stage of cycles

25
Q

what do antimitotic antibiotics do?

anthracyclines and non-anthracyclines

A
  • intercalate and inhibit DNA and RNA synthesis
  • membrane binding and increase permeability to various ions
  • Free radicals disrupt DNA chain and prevent mitosis
  • alkylation blocking DNA replication
26
Q

Which cell cycle phase do antimetabolites affect?

A

S phase

27
Q

what cell cycle phase do mitotic inhibitors affect?

A

M phase

28
Q

what are the two mitotic inhibitors which affect microtubule/spindle formation?

A
  1. taxoids

2. vinca alcaloids

29
Q

what is the aim of combination therapy?

A

increases efficacy (produces desired result) but needs to be a balanced act between keeping patient safe and treating cancer

30
Q

what 2 principles need to be considered when looking at combination chemotherapy?

A
  1. different mechanism of action (one which reduces risk of developing disease and is a synergistic/additive/positive effect )
  2. dissimilar toxicity profile (e.g. not both with neurotroxicity and give each to max. tolerated dose)
31
Q

what do antibiotics act on?

A

DNA and RNA synthesis

32
Q

what are possible side-effect of chemotherapy?

A
  • sterility
  • alopecia (hair loss)
  • pulmonary fibrosis
  • cardiotoxicity
  • local reactions
  • renal failure
  • myelosuppression (less immunity)
  • phlebitis (blood clotting)
  • neuropathy (problem with nerves)
  • myalgia (muscle pain)
  • cystisis
  • nausea/vomiting
  • mucositis (inflammation and ulceration of mucous membranes)
33
Q

what are 2 other forms of systemic therapy other than chemotherapy?

A
  1. hormonal drugs

2. targeted drugs

34
Q

what are some examples of hormonal drugs? (3)

A
  1. anti-oestrogen (Tamoxifen) aromatase inhibitors for breast cancers
  2. Gonadorelin analogue e.g. Goseralin (Zoladex)
  3. anti-androgen for prostate cancer (CPA, flutamide)
35
Q

what are some examples of receptors target drugs act on?(2)

A
  • EGFR

- VEGF

PoD topics (34 decks)

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