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Pharmacology 2 > Chemotherapy > Flashcards

Chemotherapy Flashcards

0
Q

What are the three compartments cells occupy in a solid tumour?

A

A - dividing cells
B - resting cells capable of dividing
C - cells no longer divide but contribute to tumour volume

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1
Q

What are the three objectives of cancer therapy?

A

Curing patient
Prolonging life
Palliative therapy

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2
Q

Which cells are the only ones susceptible to most cytotoxic drugs?

A

Compartment A

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3
Q

What is the aim of chemotherapy?

A

To kill all malignant cells in the body

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4
Q

Give 8 toxic effects of chemotherapy

A 
Bone marrow suppression
Impaired wound healing
Loss of hair
Damage to GI epithelium 
Growth stunted
Reproductive system - sterility
Teratogenicity - effect development of foetus
Nausea and vomiting
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5
Q

What are two possible targets for anti cancer drugs?

A

Hormonal regulation of tumour growth

Defective cell cycle controls

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6
Q

What are the four classes of anti cancer drugs?

A

Cytotoxic
Hormones
Monoclonal antibodies
Protein kinase inhibitors

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7
Q

What do alkylating agents target?

A

Cells in S phase

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8
Q

How do alkylating agents work?

A

Form covalent bonds with DNA, prevent uncoiling, inhibits replication.

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9
Q

What are the side effects with prolonged use of alkylating agents?

A

Sterility (esp men), increased risk of non lymphocytic leukaemia.

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10
Q

What are the 4 classes of alkylating agents?

A

Nitrogen mustards
Nitrosoureas
Platinum compounds
Others

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11
Q

What is the name of the first anti cancer drug?

A

Mechlorethamine

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12
Q

How are nitrogen mustards given and why?

A

IV - very reactive

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13
Q

Give 5 examples of nitrogen mustards?

A

Cyclophosphamide, melphalan, chlorambucil, bendamustine, estramustine.

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14
Q

How is cyclophosphamide administered and activated?

A

Orally, activated by liver.

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15
Q

What is estramustine reliant on?

A

Testosterone

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16
Q

What can nitrosoureas do?

A

Cross blood brain barrier - highly lipophilic. Treatment for CNS tumours.

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17
Q

Name 2 nitrosoureas and how they would be administered.

A

Carmustine (BCNU) IV

Lomustine (CC NU) given orally

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18
Q

What type of drug is cisplatin?

A

Platinum compound

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19
Q

Is cisplatin potent?

A

Yes

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20
Q

How does cisplatin work?

A

Binds to RNA Increase DNA and protein, binds to purine bases.

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21
Q

What may develop when using cisplatin?

A

Resistance

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22
Q

Which cancers are more sensitive to cisplatin?

A

Testicular/ovarian cancer

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23
Q

How is cisplatin given?

A

Slow IV injection/infusion

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24
Q

What are the side effects of cisplatin?

A

Very nephrotoxic
Severe nausea/vomiting
Risk of tinnitus, peripheral neuropathy, hyperuricemia (gout) and anaphylaxis

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25
Q

What other platinum compound is derived from cisplatin but gives less side effects and can be given as an outpatient?

A

Carboplatin

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26
Q

What is the problem with carboplatin?

A

More myelotoxic - damages bone marrow

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27
Q

Which platinum compound is used to treat colorectal cancer with fluorouracil and folinic acid?

A

Oxaliplatin

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28
Q

What is busulfan?

A

A leukaemia treatment selective for bone marrow alkylating agent.

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29
Q

What is procarbazine?

A

A alkylating agent used to treat Hodgkin’s disease

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30
Q

What is a side effect of procarbazine?

A

Can cause hypersensitivity rash and inhibits MAO as enzyme breaks down noradrenaline and dopamine.

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31
Q

What is trabectedin?

A

Alkylating agent used to treat soft tissue sarcoma and advanced ovarian cancer

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32
Q

What is a side effect of trabectedin?

A

Hepatotoxic

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33
Q

How do antimetabolites work?

A

Folate antagonists - cells cannot divide/no DNA synthesis.

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34
Q

Which antimetabolite inhibits dihydrofolate reductase?

A

Methotrexate

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35
Q

How would you give methotrexate?

A

Orally, IM, IV or intrathecally.

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36
Q

Does methotrexate cross the bbb?

A

No

37
Q

Who should have a lower dose of methotrexate?

A

Renal impairment

38
Q

Whichever drugs can reduce the excretion and thus increase toxicity of methotrexate
?

A

NSAID’s

39
Q

What is methotrexate given with in high doses to rescue normal cells?

A

Folinic acid

40
Q

What other condition is methotrexate used in to suppress the immune system?

A

Rheumatoid arthritis

41
Q

What do pyrimidine analogues compete with?

A

C and T bases

42
Q

What do pyrimidine analogues inhibit?

A

DNA synthesis

43
Q

List 4 pyrimidine analogues

A

Fluorouracil, capecitabine, cytarabine and gemcitabine

44
Q

How are pyrimidine analogues given?

A

Parenterally

45
Q

What do purine analogues compete with?

A

A and G bases

46
Q

What do purine analogues inhibit?

A

Purine metabolism

47
Q

Give 3 examples of purine analogues

A

Mercaptopurine/tioguanine, pentostatin and fludarabine.

48
Q

Mercaptopurine/tioguanine is mainly used for what treatment?

A

Leukaemia treatment

49
Q

What is doxorubicin and how does if work?

A

Cytotoxic antibiotic, binds to DNA and inhibits DNA/RNA synthesis. Inhibits topoisomerase 2

50
Q

How is doxorubicin given?

A

By IV infusion

51
Q

What are the problems with doxorubicin?

A

Dissolves the tissues of the skin.

Can cause dysrhythmias/heart failure in high doses.

52
Q

What is bleomycin?

A

Cytotoxic antibiotic

53
Q

How does bleomycin work?

A

Degrades pre formed DNA. Active against non-dividing cells.

54
Q

What are the bad effects of bleomycin?

A

Causes pulmonary fibrosis in 10% patients. 50% patients develop mucocutaneous reactions such as mouth sores, hair loss, fungal infections and hyperpyrexia.

55
Q

Which cytotoxic antibiotic is used in the treatment of paediatric cancers?

A

Dactinomycin

56
Q

Vinka alkoids are a type of what?

A

Plant derivative

57
Q

Give 3 examples of vinka alkoids?

A

Vincristine, vinblastine, vindesine

58
Q

What are vinka alkoids derived from?

A

Madagascar periwinkle

59
Q

What do vinka alkaloids prevent?

A

•Prevent polymerisation of tubulin → microtubules → prevents spindle formation

60
Q

When can the effects of vinka alkaloids occor?

A

Only during mitosis M phase

61
Q

Vinka alkaloids are relatively non toxic except for?

A

Vincristine - neuromuscular effects

62
Q

Give two examples of taxanes

A

•E.g. paclitaxel, docetaxel

63
Q

paclitaxel, docetaxel are derived from what and used to treat what?

A

Yew tree.

Breast cancer.

64
Q

paclitaxel/ carboplatin are used to treat…

A

Ovarian cancer

65
Q

Etoposide is derived from what?

A

The mandrake root

66
Q

Etoposide is used to treat what?

A

Testicular cancer/lymphomas

67
Q

Etoposide must avoid what?

A

Skin contact

68
Q

What can Etoposide cause?

A

A rapid fall in blood during IV Infusion

69
Q

Which cancers are hormones used to treat?

A

•Used in treatment of cancers in hormone-sensitive tissues (e.g. breast, prostate, ovaries)

70
Q

How do hormones work?

A

Tumour growth inhibited by R antagonists, hormones with opposing actions, or drugs which block synthesis of endogenous hormones

71
Q

How do oestrogens work?

A

Antagonists androgen dependent prostate cancer

72
Q

What are the side effects of oestrogens?

A

Nausea, fluid retention, thrombosis: impotence and gynaecomastia

73
Q

Name 3 other hormones used in cancer treatment

A

Progesterones
GnRH analogues
Somatostatin analogues

74
Q

What type of drug is tamoxifen?

A

A hormone antagonist

75
Q

How does tamoxifen work?

A

•Competitive antagonist at oestrogen Rs → inhibits transcription of oestrogen-responsive genes → breast cancer treatment

76
Q

What are the adverse effects of tamoxifen?

A

•Adverse effects: similar to menopausal effects, may cause endometrial cancer + ↑ risk of blood clots

77
Q

What are •Letrozole/ exemastine and how do they work?

A

•Aromatase inhibitors

Block conversion of androgens to oestrogens

78
Q

What are •Flutamide, cyproterone, bicalutamide

And which cancer are they used to treat?

A

Androgen antagonists - prostate cancer

79
Q

•Prednisolone/ dexamethasone work by and are used for?

A

Inhibit lymphocyte proliferation → treatment of lymphomas/ leukaemias.
•Counter some side-effects of other anti-cancer drugs (e.g. nausea/ vomiting)
•i.e. used as supportive therapy/ in palliative care

80
Q

What are Monoclonal antibodies

A
  • Produced by cultured hybridoma cells
  • React with specific target proteins expressed on cancer cells → activates immune system → lysis of cancer cells
  • Some mAbs activate GF-Rs on cancer cells → inhibit survival/ promote apoptosis
81
Q

What are the advantages of Ma’s?

A

•Advantages: targeted therapy → fewer side-effects

82
Q

What are the disadvantages of Ma’s?

A

•Disadvantage: expensive; must be given in combination with other drugs

83
Q

How does rituximab work?

A

Binds to CD20 protein, expressed on certain lymphoma cells → lysis of B-lymphocytes

84
Q

What are the disadvantages of rituximab?

A

•Not all tumours have CD20
Can cause hypotension, chills + fever
•Longer term – hypersensitivity (can be fatal)

85
Q

How does herceptin work?

A

•Binds to HER2 factor

Induces immune resp. + cell cycle inhibitors

86
Q

Imatinib is a type of?

A

Protein kinase inhibitor

87
Q

How does imatinib work?

A

Blocks tyrosine kinases involved in GF signaling pathways

88
Q

Cytotoxic drugs often given in combination – why?

A
  • ↑ cytotoxicity without ↑ general toxicity (i.e. drugs have diff. side-effects)
  • ↓ chance of developing resistance to individual drugs
89
Q

Cytotoxic drugs Often given in large doses every 2-3 weeks (usually over 6 months) – why?

A
  • allows bone marrow to regenerate ↓ chance of developing resistance to individual drugs
  • more effective than several small doses
90
Q

How can you control the side effects of chemotherapy?

A

Control of side-effects
Nausea + vomiting (emesis)
•↓ patient compliance
•Ondansetron/ granisetron – 5HT3R antagonists → effective vs cytotoxic drug-induced vomiting
•Metoclopramide – dopamine (D2R) antagonist
0
Anxiety
•Lorazepam - anti-anxiety drug (Benzodiazepine)

Myelosuppression
•Stem cell transplant
–Autologous: stem cells harvested* from patient + infused back after chemotherapy
–Allogenic: stem cells from a matched donor
i.e. collected from blood (by dialysis) or bone marrow

Pharmacology 2 (14 decks)

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