cancer chemotherapy Flashcards

(39 cards)

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

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
examples of antimetaboltes
folates purine prymidine .... antagonists
26
folic acid antagonist
methotrexate - interferes with formation od DNA RNA and cellular proteins prolongs inhibitor effect as her to metabolise immunosuppressive, cytotoxic and anti inflammatory
27
purine anatagnost
6 mercaptopurine must be metabolised into active form alters synthesis of DNA/rNA nausea vomiting pain abdomanal
28
pyrimidine anatagnoist
flurouracil requires activation to interfere with DNA synthesis short half life nausea, vomiting, headache, mood disorder
29
vinca alkaloids and what type of drug are they
CCS inhibits tunilin proliferation microtubules not assembles cell death from mitosis arrest eg vincacrystine
30
vincristine main dose limiting toxicity
neurotoxicity
31
taxanes and type of drug
CCS Enhance tubular polymerisation inhibition of mitosis and cell division eg palcitaxel
32
paclitaxel
used in slid tumours | dose reduction required in pts with liver diseases to prevent accumulation
33
antitumoru antiiotics
abnormality in the cell proliferation | - block synthesis, DNA strand scission, interfere with cell repliation
34
doxorubicin
generates free radicals leading to cardiotoxiciyt
35
hormones and anatagonists
glucocorticoids - estrogens - antagonists of androgens estrogens antagonists - ER modulators
36
what is given to its with bone metastats
bisphosphonates slow down rate of growth of bone crystal reduce morbidity by reducing skeletal vents
37
when does metastasis in skeleton occur
in its with multiple myeloma and metastatic breast prostate, thyroid cancer
38
drug combination
provide maximal cell kill within a range of toxicity tolereted by the host for each drug without dose comprmose
39
drug resistance
- some tumours exhibit primary resistance | - acquire resistance develops in response to exposure to a given anticancer agent