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Cancer kanser wtv > chemo agents > Flashcards

chemo agents Flashcards

1
Q

What are the 8 classes of Chemo agents?

A

Alkylating, Anti-metabolite, Enzyme Inhibitors, Anti-microtubules, Endocrine Therapies, Targeted therapies, Immunotherapy, Miscellaneous

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2
Q

What are the stages of the cell cycle?

A

1) Growth (G)
2) Synthesis (S)
3) Growth and preparation for mitosis (G1)
4) Cell division stage (M)

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3
Q

What kind of cells do cell-cycle specific agent kill?

A

They preferentially kill proliferating cells

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4
Q

How are cell-cycle specific agents administered?

A

Via continuous infusion to allow for exposure to more cells

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5
Q

What kinds of cells do cell-cycle non specific agents kill?

A

Malignant and non-malignant cells

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6
Q

Cell kill of cell-cycle non specific agent is proportionate to ____?

A

Dose

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7
Q

What are the examples of acute toxicities caused by chemo?

A

Bone marrow suppression, Alopecia, Mucositis

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8
Q

What kind of tissues are most vulnerable to acute toxicities?

A

Tissues with fast renewal cells such as bone marrow, skin, hair, GI mucosal cells

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9
Q

What cause acute toxicities?

A

Inhibition of host cell division

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10
Q

What are the examples of delayed toxicities caused by chemo?

A

Infertility
Anthracycline induced cardiotoxicities
MTX-induced pneumonitis

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11
Q

Examples of alkylating agents?

A

Platinum analogues, Cyclophosphamide, Ifosfamide

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12
Q

Examples of Platinum analogues?

A

Cisplatin (1st gen)
Carboplatin (2nd gen)
Oxaliplatin (3rd gen)

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13
Q

MOA of alkylating agents?

A

1) Formation of positively charged carbonium ion that binds to electron-rich sites on biomolecules
2) Binding to reactive molecules on the DNA (N-7 of guanine)
3) DNA mispairing
4) DNA strand breakage
5) Inhibition of DNA transcription and replication

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14
Q

Dose limiting toxicities of Alkylating agents?

A

Myelosuppression, nadir in 6-10 days, recovery in 14-21 days

Exception: Nitrosourea demonstrate delayed nadir and recovery.

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15
Q

Do alkylating agent show cross resistance?

A

No, can switch to different class of alkylating agent if one is ineffective

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16
Q

Alkylating agents differ greatly in?

A

PK, Lipid solubility, chemical reactivity and properties of membrane transport

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17
Q

Cyclophosphamide is activated in ____?

A

The liver

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18
Q

What are the products of cyclophosphamide activation?

A

Enzymatic: Carboxyphosphamide (Inactive)

Non-enzymatic: Acrolein, Phosphoramide mustard

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19
Q

Main cytotoxic agent of cyclophosphamide?

A

Phosphoramide mustard

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20
Q

Typical dose of cyclophosphamide? Indicated for?

A

600-750 mg/m^2

Indicated for lymphomas, breast cancer

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21
Q

High dose of cyclophosphamide? Indicated for?

A

2g/m^2

Indicated for bone marrow transplant

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22
Q

Toxicities of Cyclophosphamide?

A

N/V
Haemorrhagic cystitis
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

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23
Q

Cyclophosphamide is excreted via?

A

Urine as active/ inactive metabolites

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24
Q

Ifosfamide is activated in ____?

A

Liver via CYP3A4

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25
Q

MOA of Ifosfamide?

A

Cytotoxic activity arise from cross-linking of DNA by alkylation at N-7 of guanine. Inter-intra cross links in DNA causes cell death

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26
Q

Active metabolite of Ifosfamide?

A

Isophosphoramide mustard

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27
Q

Ifosfamide must be co-administered with?

A

Mesna

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28
Q

What is Mesna?

A

Mesna is a radical scavenger, must be administered with large dose of Ifosfamide

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29
Q

Toxicities of Ifosfamide?

A

Dose limiting haemorrhagic cystitis
Nephrotoxicity
N/V
CNS toxicity

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30
Q

MOA of platinum analogues?

A

Formation of reactive electrophile that covalently binds to DNA

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31
Q

Toxicities of Cisplatin?

A

1) Dose-limiting acute and delayed CINV
2) Cisplatin-induced Nephrotoxicity
3) Ototoxicity (may be irreversible)
4) Peripheral neuropathy (reversible)

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32
Q

When is the use of Cisplatin not recommended?

A

When patient’s SCr < 1.5 mg/dl

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33
Q

Preventive measures for Cisplatin-induced nephrotoxicity?

A

1) Avoid in patients with renal dysfunction
2) Hydration with at least 1.2L 0.9% NaCl IV pre and concurrent with Cisplatin, with Potassium and Magnesium supplementation
3) Use of osmotic diuretics (Mannitol/ Furosemide)
4) Maintain urine output >100ml/h
5) Prolong infusion time
6) Use amifostine (radical scavenger)

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34
Q

Disadvantages of Amifostine?

A

1) Expensive and myelosuppressive.

2) Might affect efficacy of Cisplatin

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35
Q

How is Carboplatin dosed?

A

Based on Calvert’s equation

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36
Q

State the Calvert’s equation

A

Dose = AUC * (GFR +25), where AUC=2 for weekly dosing, AUC= 5 or 6 for every 3 weekly dosing

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37
Q

Toxicity of Carboplatin?

A

Dose limiting myelosuppression, hypersensitivity

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38
Q

Benefits of Carboplatin over Cisplatin?

A

Carboplatin has lower incidence of Nephrotoxicity, delayed N/V, Ototoxicity

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39
Q

Indication of Cisplatin, Carboplatin, Oxaliplatin?

A

Cisplatin/ Carboplatin: Large range of solid tumour

Oxaliplatin: Colorectal cancer

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40
Q

Oxaliplatin is only stable in?

A

D5W

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41
Q

Toxicity of Oxaliplatin

A

1) Cumulative peripheral neuropathy
2) Myelosuppression
3) Nephrotoxicity
4) Hypersensitivity

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42
Q

What are the enzymes that enzyme inhibitors anatagonise?

A

Topoisomerase I and II

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43
Q

Topoisomerase I inhibitors?

A

Irinotecan (CPT-11)

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44
Q

Which stage of the cell cycle does Irinotecan affects?

A

S phase

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45
Q

Active metabolite of Irinotecan

A

SN-38

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46
Q

MOA of Irinotecan

A

Binds to Topoisomerase I-DNA complex, prevents the relegation of DNA. Resulting in DNA breakage and cell death

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47
Q

Indication of Irinotecan?

A

Metastatic colorectal cancer

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48
Q

Excretion of Irinotecan?

A

Biliary and urinary

49
Q

Toxicities of Irinotecan?

A

1) Dose-limiting Diarrhoea
2) Cholinergic syndrome
3) UGT1A1 deficiency

50
Q

Management of Irinotecan dose-limiting diarrhoea?

A

Use Loperamide 4mg at earliest sign, 2mg q2h until diarrhoea free for 12 hours

51
Q

Describe UGT1A1 deficiency

A

Patient with homozygosity for UGT1A1*28 allele has problem clearing the active metabolite SN-38

52
Q

Management of Irinotecan cholinergic syndrome?

A

Routinely pre-med with IV/SC Atropine (0.25-1 mg)

53
Q

Topoisomerase II inhibitors?

A

Etoposide, Anthracyclines

54
Q

Examples of Anthracyclines?

A

1) Doxorubicin
2) Daunorubicin
3) Epirubicin
4) Idarubicin
5) Liposomal Daunorubicin
6) Mitoxantrone

55
Q

Indication for Etoposide?

A

Wide range of solid tumour?

56
Q

Availability of Etoposide?

A

IV (100mg injection), Oral (50mg Caplet)

57
Q

Administration instructions for IV Etoposide?

A

1) Infused for at least 1 hour to avoid hypotension
2) Use non-PVC tubing
3) Diluted to concentration of <0.4mg/ml

58
Q

Toxicities of Etoposide?

A

1) Dose-limiting myelosuppression

2) Hypotension if infused too quickly

59
Q

MOA of Anthracyclines?

A

1) Induce formation of covalent topoisomerase II-DNA complexes, preventing relegation of DNA
2) Intercalation of base pairs in DNA
3) Metabolized in liver to form oxygen rich radicals

60
Q

Toxicities of Anthracyclines?

A

1) Anthracycline-induced cardiotoxicity
2) Dose-limiting myelosuppression (primarily neutropenia)
3) Alopecia
4) Acute N/V
5) Vesicant
6) Red discolouration of urine

61
Q

Before initiation of Anthracyclines what test must be performed?

A

Baseline MUGA/ECHO performed to evaluate left ventricular ejection fraction (LVEF).

If LVEF <40%, do not start

62
Q

What causes Anthracycline-induced cardiotoxicity?

A

Formation of free radicals

63
Q

Risk factors of Anthracycline-induced cardiotoxicity?

A

1) Cumulative doses
2) Age
3) Pre-existing cardiac disease
4) Administration schedule
5) Mediastinal radiation

64
Q

Prevention of Anthracycline-induced cardiotoxicity?

A

1) Limit cumulative dose, involves lifetime tracking
2) Adjust administration schedule. Fractionate doses and prolong infusion
3) Use less cardiotoxic alternative such as Liposomal Daunorubicin, Mitoxantrone
4) Use Dexrazoxane, a cardiac protectant

65
Q

Examples of Antimetabolites?

A

Anti-folate agent: MTX

Pyrimidine analogues: 5-FU, Capecitabine

66
Q

MOA of MTX?

A

Binds to Dihydrofolate reductase, prevents formation of tetrahydrofolate from folic acid. Hence, preventing formation of thymidylate and purines.

Lesser DNA synthesis, repair and cellular replication

67
Q

Indication of MTX?

A

All cancers

68
Q

Administration instructions for high dose (>1g/m^2) MTX?

A

Requires therapeutic drug monitoring and folinic acid rescue.

69
Q

What kinds of drugs should be avoided with MTX?

A

1) NSAIDs
2) Penicillins
3) Salicylates
4) Omeprazole
5) Ascorbic acid (Vit C)
6) Probenecid, Sulfonamides

70
Q

Excretion of MTX

A

Primarily renal via glomerular filtration and active tubular secretion

71
Q

Toxicities of MTX?

A

1) Dose limiting myelosuppression
2) MTX-induced pneumonitis
3) Nephrotoxicity
4) Hepatitis
5) Diarrhoea
6) Mucositis
7) CNS toxicities
8) MTX can escape into third spaces. Patients with ascites, pleural effusion are at high risk for MTX toxicity

72
Q

MOA of 5-FU?

A

Acts as a “false pyrimidine”, inhibits the enzyme Thymidylate synthase, thus inhibiting formation of the DNA base thymidine

73
Q

Indication of 5-FU?

A

Solid tumour cancers

74
Q

Excretion of 5-FU

A

As respiratory CO2, and via biliary system

75
Q

Toxicities of 5-FU

A

Depends on the duration and rate of administration

1) Dose-limiting leukopenia, thrombocytopenia, anemia in bolus administration
2) Dose-limiting hand-food symptoms and diarrhoea in continuous infusion
3) Skin discolouration
4) Nail changes
5) Photosensitivity
6) Neurologic toxicities
7) Vasospastic angina

76
Q

MOA of Capecitabine?

A

Undergoes 3-step conversion to fluorouracil. Last step being phosphorylation by thymidine phosphorylase (TP). TP is found in higher levels in tumour cell

77
Q

Indication of Capecitabine?

A

Solid tumour cancers

78
Q

Toxicities of Capecitabine?

A

1) Dose-limiting hand foot syndrome (more in Capecitabine), mucositis, diarrhoea
2) CINV
3) Fatigue
4) Rash

79
Q

Examples of Anti microtubule drug?

A

Vinca alkaloids, Taxanes

80
Q

Examples of Vinca alkaloid?

A

Vincristine, Vinblastine, Vinorelbine

81
Q

Examples of Taxanes?

A

Paclitaxel, Docetaxel

82
Q

MOA of Vinca?

A

Inhibition of polymerisation by binding to Tubulin

83
Q

MOA of Taxanes?

A

Inhibition of depolymerisation by binding to microtubules

84
Q

Toxicities of Vinca (general)?

A

1) Alopecia

2) Vesicants

85
Q

Benefit of Vinca?

A

Low emetogenic potential

86
Q

Toxicities of Vincristine?

A

1) Peripheral neuropathy
2) Ileus
3) Constipation

87
Q

Toxicities of Vinblastine, Vinorelbine?

A

1) Dose-limiting neutropenia, thrombocytopenia
2) Neurologic toxicity
3) Constipation

88
Q

Premedication for Paclitaxel? Indicated for?

A

To prevent Hypersensitivity. Anti-histamines (H1 & H2), Corticosteroids

89
Q

Premedication for Docetaxel? Indicated for?

A

To prevent Edema. Dexamethasone 8mg PO BD, start 1 day prior to treatment, continuing for 2 additional days

90
Q

Toxicities of Paclitaxel?

A

1) Hypersensitivty
2) Myelosuppression (Less significant than Docetaxel)
3) Myalgias
4) Peripheral neuropathy
5) Mucositis (Seen more with prolonged infusion)

91
Q

Toxicities of Docetaxel?

A

1) Myelosuppression (Neutropenia more significant than Paclitaxel)
2) Less peripheral neuropathy
3) Less hypersensitivity
4) Less asthenia

92
Q

Examples of Endocrine therapies?

A

1) Antiestrogen

2) Anti-aromatase

93
Q

Example of Antiestrogen agent?

A

Tamoxifen, a selective estrogen receptor modulator.

94
Q

Indications for Tamoxifen?

A

1) Indicated for pre menopausal women with Estrogen-receptor positive breast cancer.
2) Advanced endometrial cancer

95
Q

MOA of Tamoxifen?

A

Inhibits nuclear binding of the estrogen receptor, prevent estrogen from stimulating breast cancer cells

96
Q

Antagonist and Agonist activity of Tamoxifen?

A

Antagonist: Breast epithelial cells (Cancer/ Non cancer)
Agonist: Bone, Lipids, Endometrium (Can increase risk for endometrium cancer)

97
Q

Examples of Anti-aromatase agent?

A

1) Anastrozole
2) Letrozole
3) Exemestane

98
Q

Group of patient anti-aromatase agent is used in?

A

Post-menopausal women

99
Q

SEs of Anti-aromatase agents?

A

1) Hot flashes
2) Fatigue
3) Myalgia/ Arthralgia
4) Bone Loss

100
Q

Two major classification of Targeted Therapies?

A

1) Small molecular drug

2) Monoclonal antibodies

101
Q

TT-induced toxcities?

A

1) Cardiotoxicity
2) Neurotoxicity
3) Immunotoxicity
4) Hepatotoxicity
5) Pulmonary toxicity
6) GI toxicity
7) Dermatological toxicity

102
Q

Examples of Small molecule drugs?

A

Epidermal growth factor tyrosine kinase inhibitors:

1) Gefitinib
2) Erlotinib
3) Afatinib

103
Q

MOA of Epidermal growth factor tyrosine kinase inhibitors

A

Inhibits cell proliferation by blocking intracellular signals that stimulate gene expression.

1) Decrease proliferation
2) Decrease cell survival
3) Decrease growth factor
4) Decrease angiogenesis
5) Decrease metastasis
6) Increase Chemo/Radio sensitivity

104
Q

Epidermal growth factor tyrosine kinase inhibitors are indicated for?

A

EGFR positive cancers (Lung, pancreatic (erlotinib only))

105
Q

Toxicities of small molecule drugs?

A

1) Dermatological toxicities (Mild)

2) Diarrhoea

106
Q

Management principle for toxicities of small molecule drugs?

A

1) Should not interfere with anti-tumour effects of EGFR-inhibitors
2) Minimal SEs
3) Tailored to type of clinical presentation

107
Q

What are the agents used for dermatological toxicities?

A

1) Anti-microbials
2) Emollients/ Skin protectant
3) Antihistamines
4) Retinoids
5) Corticosteroids/ Immunomodulators

108
Q

Examples of Monoclonal antibodies?

A

1) Rituximab
2) Bevacizumab
3) Trastuzumab

109
Q

MOA of Rituximab?

A

Binds to CD20 receptors on malignant/ normal B cells leading to:

1) Apoptosis
2) Complement Dependent Cytotoxicity
3) Antibody-dependant cell-mediated cytotoxicity

110
Q

Toxicities of Rituximab?

A

1) Infusion related reactions (Fever, chill/rigor, bronchospasm, hypotension)
2) N/V
3) Myelosuppression
4) Infections

111
Q

Management of Infusion related reactions?

A

1) Pre-medicate with paracetamol, diphenhydramine

2) Start infusion slow and increase rate overtime

112
Q

MOA of Bevacizumab?

A

Vascular endothelial growth factor inhibitor

113
Q

Bevacizumab should be avoided in _____?

A

Patient with bleeding risk, CNS metastasis

114
Q

MOA of Trastuzumab?

A

HER2/ Neu receptor antagonist

115
Q

Indication for Trastuzumab?

A

Cancer with HER2 overexpression (Breast/ Gastric)

116
Q

Toxicities of Trastuzumab?

A

Cardiotoxicity, hypersensitivity

117
Q

Toxicities of Bevacizumab?

A

1) Increased risk of thrombotic events (Stroke)
2) Haemorrhage
3) Gastrointestinal perforation
4) Proteinuria
5) Wound healing complication

118
Q

Examples of Immunotherapies?

A

1) Ipilimumab
2) PD-1 inhibitor
3) PD-L1 inhibitor

119
Q

MOA of Ipilimumab?

A

Blocks cytotoxic T-cell lymphocyte associated antigen (CTLA-4) inhibitory signal, allowing CTL to kill cancer cells

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