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Pharmacology 4090 > Anticancer Drugs > Flashcards

Anticancer Drugs Flashcards

1
Q

Cancer that causes the most deaths in both sexes

A

Lung cancer

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2
Q

Overall trend of cancer death rates in recent years

A

Decreasing

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3
Q

Most common cancer treatments

A

Surgery, radiation, chemo

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4
Q

Goal of anticancer drugs

A

To destroy all cancer cells

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5
Q

3 main functions of anticancer drugs

A

Act on DNA, inhibit chromatin function, act on hormone receptors

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6
Q

Carcinoma

A

Cancer of epithelial cells

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7
Q

Sarcoma

A

Cancer of muscle, bone, cartilage, fat, connective tissue

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8
Q

Leukemia

A

Blood cancers that originate in bone marrow and result in underdeveloped blood cells

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9
Q

Lymphoma

A

Group of cancers in lymphocytes

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10
Q

Blastoff

A

Cancer in precursor cells

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11
Q

Cancer cell stages

A

Initiation, promotion, progression

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12
Q

Tumour progression depends on

A

Mutation/epigenetic alteration rate, selective advantage, proliferation rate, invasiveness

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13
Q

Critical cancer genes

A

DNA repair genes, genes maintaining chromosome integrity, oncogenes, tumour suppressor genes

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14
Q

3 outcomes of a diseased cell

A

Apoptosis, senescence, cancer

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15
Q

Oncogene

A

Normally increases mitosis; can become constitutively active

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16
Q

Tumour suppressor genes

A

Normally suppress mitosis; can lose function

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17
Q

Angiogenesis

A

Tumours secrete growth factors to induce blood vessel growth

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18
Q

Metastasis

A

Detachment from parent tumour → enter blood vessel → proliferate in new environment

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19
Q

When chemotherapy is used

A

In addition to radiation or surgery, to cure, in palliative care

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20
Q

What cells anticancer drugs are most effective against

A

Rapidly dividing cells

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21
Q

Cell cycle checkpoints

A

G1, g2, metaphase

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22
Q

G1 checkpoints

A

Checks for nutrients, growth factors, and DNA damage to make sure all is ready to synthesize

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23
Q

G2 checkpoint

A

Checks for cell size and DNA replication

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24
Q

Metaphase checkpoint

A

Checks for chromosome spindle attachment

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25
Q

When drugs are most toxic in the cell cycle

A

S Phase, some also M

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26
Q

Growth fraction

A

The percent of dividing cells that are sensitive to chemotherapy

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27
Q

What phase of the cell cycle most drugs are ineffective in

A

G0

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28
Q

Debulking

A

Shrinking tumour, which stimulates proliferation

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29
Q

Early metastases

A

Have a high growth fraction

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30
Q

Use of several chemo cycles

A

Synchronizes cells

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31
Q

Log kill

A

Amount of cells that are killed in each treatment due to first order kinetics

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32
Q

Therapeutic index of anticancer drugs

A

Very narrow

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33
Q

Factors that influence patient survival

A

Nature of the cancer, pharmacology, patient

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34
Q

Causes of failure of anticancer drugs

A

Lack of specificity and resistance

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35
Q

Major sites of toxicity of anticancer drugs

A

Bone marrow, gi tract, hair follicle, reproductive tract, 2° carcinogenicity

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36
Q

Resistance to anticancer drugs

A

Natural, acquired, or multi drug resistance

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37
Q

Treatment regimen of chemo

A

Usually given in combination, as frequently and as close to maximal effective dose as possible

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38
Q

Dosage is based on

A

Body surface area, pharmacokinetics, interactions, impacts on systems

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39
Q

Considerations for chemotherapy

A

Long-term gain versus risk, successful treatment versus qualify of life

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40
Q

Cyclophosphamide mechanism of action

A

Transfers an alkyl group to N7 or O6 of guanine to one or two DNA strands, resulting in monoalkylated or crosslinked strands

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41
Q

Cells most sensitive to cyclophosphamide

A

Proliferating cells

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42
Q

Most commonly used alkylating agent

A

Cyclophosphamide

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43
Q

Cyclophosphamide routes of admin

A

Oral or IV

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44
Q

Fates of aldophosphamide

A

To the cytotoxic phosphoramide mustard that binds the DNA, or to acrolein - toxic metabolite

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45
Q

Glutathione-s-transferase

A

Inactivates aldophosphamide products to nontoxic

46
Q

Adverse effects of cyclophosphamide

A

Gi distress, bone marrow suppression, immunosuppression, alopecia, hemorrhagic cystitis, sterility, menopause, cancer * is less toxic than other agents due to ALDH tho*

47
Q

Resistance to cyclophosphamide

A

Increased ALDH or GST, increased DNA repair (mgmt)

48
Q

Cisplatin mechanism

A

Covalently binds N7 and O6 on guanine via a metal, but can also binds cytosine and adenine

49
Q

Admin of cisplatin

50
Q

Adverse effects of cisplatin

A

Bone marrow suppression, anemia, severe nausea and vomiting, nephrotoxicity, electrolyte imbalance, neurotoxicity

51
Q

Cisplatin resistance

A

Increased metabolism by GST or increased efflux, less access into cell, increased DNA repair

52
Q

Bleomycin mechanism

A

Forms a complex with DNA and iron that gets oxidized to form free radicals → DNA strand breakage

53
Q

Bleomycin admin

A

IV, IM, SC

54
Q

Resistance to bleomycin

A

Increased DNA repair, increased efflux, increased antioxidants, increased bleomycin hydrolase

55
Q

Adverse effects of bleomycin

A

Pulmonary fibrosis, hypersensitivity, gi distress, alopecia

56
Q

CMF

A

Cyclophosphamide, methotrexate fluorouracil

57
Q

Antimetabolites

A

Methotrexate and 5-fluorouracil

58
Q

Methotrexate mechanism

A

Is structurally similar to folate so it binds dihydrofolate reductase and prevents the synthesis of purines and pyridines, metabolites also stay in alls to further inhibit synthesis

59
Q

Routes of admin for methotrexate

A

IV, IM, SC, IT

60
Q

Resistance to methotrexate

A

Non-proliferating cells, decreased cellular uptake, increased dihydrofolate reductase expression, decreased binding to dihydrofolate reductase

61
Q

Adverse effects of methotrexate

A

Bone marrow suppression, gi distress, alopecia, liver damage, renal damage

62
Q

Drug interactions with methotrexate

A

Aminoglycosides inhibit its absorption, NSAIDs, penicillins, cephalosporins, cisplatin, probenecid decrease its elimination

63
Q

How 5-fluorouracil and methotrexate enters cells

A

Carrier- mediated transport

64
Q

5-fluorouracil mechanism

A

Gets converted to ribose and deoxyribose nucleotide metabolites and incorporated into RNA and DNA to prevent elongation, also inhibits thymidine synthesis

65
Q

Routes of admin of 5-fluorouracil

A

Iv or topically

66
Q

Adverse effects of 5-fluorouracil

A

Bone marrow suppression, gi disturbances, alopecia, cardiotoxicity, skin irritation

67
Q

Dosing concerns of 5-fluorouracil

A

Very narrow therapeutic index, under and overdosing are both concerning

68
Q

Resistance of 5-fluorouracil

A

Decreased cell uptake, increased 5-fluorouracil metabolism, decreased conversion to nucleotide metabolites, increased thymidylate synthase activity, DNA repair

69
Q

Topoisomerase inhibitors

A

Doxorubicin

70
Q

Chromatin modulators

A

Doxorubicin, vincristine, paclitaxel

71
Q

Doxorubicin mechanism

A

Binds and stabilizes topoisomerase II DNA complex to prevent re-ligation of DNA breaks; also generates free radicals

72
Q

Topoisomerase ll

A

Hydrolyses double-stranded DNA during replication and transcription, and then re-ligates it

73
Q

Routes of admin of doxorubicin

74
Q

Adverse effects of doxorubicin

A

Cardiomyopathy/HF, bone marrow suppression, gi disturbances, alopecia, swelling of hands and feet

75
Q

Resistance to doxorubicin

A

Increased efflux by p-glycoprotein, over-expression or mutation of topoisomerase lI

76
Q

Microtubule inhibitors

A

Vincristine, paclitaxel

77
Q

Vincristine mechanism

A

Inhibits tubulin polymerization

78
Q

Paclitaxel mechanism

A

Inhibits tubulin depolymerization

79
Q

Route of admin of vincristine

80
Q

Affected cell cycle stage by vincristine

81
Q

Resistance to vincristine

A

Altered tubulin structure, altered tubulin isotopes, increased efflux by p-glycoprotein

82
Q

Adverse effects of vincristine

A

Peripheral neuropathy, nausea, vomiting, alopecia, constipation

83
Q

Interactions of vincristine

A

Metabolized by CYP3A4, so it’s metabolism is accelerated by HIV meds and anticonvulsants, and slowed by azoles, other HIV meds, and grapefruit juice

84
Q

Adverse effects of paclitaxel

A

Hypersensitivity, peripheral neuropathy, bone marrow suppression, alopecia, gi distress and anorexia

85
Q

Interactions of paclitaxel

A

Same as vincristine

86
Q

Resistance to paclitaxel

A

Same as vincristine

87
Q

Uses for steroid hormones and antagonists

A

Cancers with steroid-hormone sensitive cells because steroids regulate genes for cell growth and proliferation

88
Q

Prednisone action

A

Binds irreversibly to glucocorticoid receptors and induces apoptosis of leukemic and lymphoid cells

89
Q

Resistance to prednisone

A

Absence or mutation of receptor

90
Q

Adverse effects of prednisone

A

Immunosuppression, hypertension, hyperglycemia, pancreatitis, weakness, osteoporosis, mood changes

91
Q

Tamoxifen mechanism

A

SERM, metabolized in liver by 3A4 and 2D6 and prevents estrogen-mediated expression and growth in breast tissue

92
Q

Resistance to tamoxifen

A

Absence or mutation of receptor

93
Q

Adverse effects of tamoxifen

A

Hot flashes, irregular periods, blood clots, reduced cognition, uterine cancer

94
Q

Anastrazole mechanism

A

Inhibit aromatase, do not induce uterine cancer

95
Q

Most immediate way to reduce cancer deaths

A

Prevention, screening, early detection

96
Q

Multi drug resistance

A

An efflux pump that affects several drugs, such as p-glycoprotein

97
Q

P-glycoprotein

A

Transmembrane atp-binding transporter that interferes w/ chemo agents

98
Q

P-glycoprotein mechanism

A

Hydrolyses ATP and releases the phosphate to shift the position of the drug and cause excretion

99
Q

_________ downregulates expression of p-glycoprotein

100
Q

________ inhibits efflux of drugs by p-glycoprotein

101
Q

__________ and __________ induce expression of p-glycoprotein

A

Cisplatin; doxorubicin

102
Q

Piperine analogs

A

Helps overcome drug resistance

103
Q

Hormone sensitive breast tumours

A

ER positive, progesterone receptor positive, hER-2 positive

104
Q

Trastuzumab mechanism

A

Antibody that acts an antagonist at HER2

105
Q

Bevacizumab mechanism

A

Antibody that acts as an antagonist at vascular endothelial growth factor receptor 2 to inhibit angiogenesis

106
Q

Adverse effects of trastuzumab

A

Fever, ache, chills, nausea, diarrhea, cardiac dysfunction including congestive heart failure

107
Q

Adverse effects of bevacizumab

A

Inhibition of blood vessel growth for maintenance and healing, hypertension, bleeding

108
Q

Olaparib mechanism

A

Inhibits PARP, which down-regulates DNA repair mechanism

109
Q

Adverse effects of olaparib

A

Bone marrow suppression, gi disturbances, anorexia, fatigue, muscle and joint pain

110
Q

Atezolizumab mechanism

A

Antibody against programmed cell death-ligand 1, which allows t cells to kill the tumour alls

111
Q

Adverse effects of atezolizumab

A

Nausea, anorexia, fatigue, UTI

Pharmacology 4090 (11 decks)

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