cancer chemotherapy Flashcards

1
Q

benign vs malignant

A

malignant capable of invading surrounding tissue

benign confined to its original location

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2
Q

causes of cancer

A

1) environmental exposure eg UV light, radiation
2) verse’s
3) oncogenes
4) tumour suppressor genes

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3
Q

treatmetns

A

surgery
radiotherapy
cehmotheraory

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4
Q

chemotherapy

A

once cancer metasies chemo required for effective cancer managment

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5
Q

what do cancer drugs vary by

A
  • chemical composition
  • route of administration
  • type of cancer targeted
  • side effects
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6
Q

chemotherapy approaches

A

primary induction chemo
neoadjuvant chemo
adjuvant chemo

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7
Q

primary induction chemo

A

administed in its with advance cancer

no alternative tx

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8
Q

neoadjuvant chemo

A

its with localised therapies where alternatives are not as effective

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9
Q

adjuvant chemo

A

as an adjuvant to local therapy

effective in prolonging both disease free and overall surviial

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10
Q

therapeutic index

A

Therapeutic index is the lethal dose of a drug for 50% of the population (LD50) divided by the minimum effective dose for 50% of the population (ED50)

want a large therapeutic index

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11
Q

what is needed for total cell kill

A

early diagnosis and tx
combination chemo
intermittent regimens
adjuvant and neoajuwant

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12
Q

what do chemotherapeutic agents

A

kill a constant proportion of tumour cell population, rather than a constant number of cells after each dose

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13
Q

solid vs disseminated cancer

A

solid cancer
- have a low growth fractions thus respond poorly to chemo and need surgical removal
disseminated
high growth fraction and respond well to chemo

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14
Q

cell cycle specific drugs

A

exhert action on cells traversing the cell cycle

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15
Q

CCNS cells

A

can sterilise tumour cells whether cycling or resting in G0

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16
Q

CCNS vs CCS

A

non specific able to block more cells as they are non specific

17
Q

what can alkylating agents o

A

CCNS

  • transfer alkyl groups to nucleophilic sites on DNA bases (form highly reactive carbonium ion)
  • cross linkage, abnormal base pairing, DNA strand breakage
18
Q

what can alkylating agents lead to

A

can alter healthy cells as interferes with cell cycle
lead to toxicity of other cells themselves
increase risk of second maliganies

19
Q

what is often given with alkylating agents

A

antiemetics

20
Q

alkylating drugs - examples

A

buluslfan
- control tumour burten
lomustine - BBB,
decarbaizine

21
Q

resistant to agents - what to do

A
  • increase activity of DNA repair enzyme
  • increase metabolic inactivation of the drug
  • decrease influx of the drug
22
Q

platinum analogues CCNS

A
thought to exhort cytotoxic effect similar to alkylating agents
- form platinum complexed 
intrastrand and inter strand cross link
DNA damge
inhibits cell proliferation
23
Q

cisplatin

A

highly bound to plasma protein
poor for BBB
extensively cleared by kidney and excrete slow

adverse effects
emesis
nephrotoxicity
p

24
Q

antimetabolites and type

A

CCs
acts on intermediary metabolism of proliferating cells
interferes with DNA/RNA growth by substituting for the normal building blocks of RNA/DAN

eg folate anatagonist - methotrexate

25
Q

examples of antimetaboltes

A

folates
purine
prymidine

…. antagonists

26
Q

folic acid antagonist

A

methotrexate
- interferes with formation od DNA RNA and cellular proteins
prolongs inhibitor effect as her to metabolise

immunosuppressive, cytotoxic and anti inflammatory

27
Q

purine anatagnost

A

6 mercaptopurine
must be metabolised into active form
alters synthesis of DNA/rNA

nausea
vomiting
pain abdomanal

28
Q

pyrimidine anatagnoist

A

flurouracil
requires activation to interfere with DNA synthesis
short half life

nausea, vomiting, headache, mood disorder

29
Q

vinca alkaloids and what type of drug are they

A

CCS
inhibits tunilin proliferation
microtubules not assembles
cell death from mitosis arrest

eg vincacrystine

30
Q

vincristine main dose limiting toxicity

A

neurotoxicity

31
Q

taxanes and type of drug

A

CCS
Enhance tubular polymerisation
inhibition of mitosis and cell division

eg palcitaxel

32
Q

paclitaxel

A

used in slid tumours

dose reduction required in pts with liver diseases to prevent accumulation

33
Q

antitumoru antiiotics

A

abnormality in the cell proliferation

- block synthesis, DNA strand scission, interfere with cell repliation

34
Q

doxorubicin

A

generates free radicals leading to cardiotoxiciyt

35
Q

hormones and anatagonists

A

glucocorticoids -
estrogens - antagonists of androgens
estrogens antagonists - ER modulators

36
Q

what is given to its with bone metastats

A

bisphosphonates
slow down rate of growth of bone crystal
reduce morbidity by reducing skeletal vents

37
Q

when does metastasis in skeleton occur

A

in its with multiple myeloma and metastatic breast prostate, thyroid cancer

38
Q

drug combination

A

provide maximal cell kill within a range of toxicity tolereted by the host for each drug without dose comprmose

39
Q

drug resistance

A
  • some tumours exhibit primary resistance

- acquire resistance develops in response to exposure to a given anticancer agent