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Pharmacotherapeutics IV CA3 > Pharmacology of Anti-Cancer Agents > Flashcards

Pharmacology of Anti-Cancer Agents Flashcards

1
Q

Which chemotherapy agents are cell cycle phase specific to the M phase?

A
  • docetaxel
  • paclitaxel
  • vinblastine
  • vincristine
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2
Q

Which chemotherapy agents are cell cycle phase specific to the S phase?

A
  • 5 FU
  • Irinotecan
  • Methotrexate
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3
Q

What cells do chemotherapy agents preferentially kill?

A

Proliferating cells

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4
Q

What cells do non specific agents eg radiation kill?

A

Both normal and malignant cells to the same extent.

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5
Q

What does each transition in the cell cycle require?

A

Activation of cyclin-dependent kinases

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6
Q

How do we allow more exposure for cell cycle phase specific agents?

A

Continuous infusion

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7
Q

What are some characteristics of cell cycle phase non specific agents?

A
  • exert cytotoxic effect throughout the cell cycle, including resting phase
  • cell kill is proportional to dose
  • examples: alkylating agents
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8
Q

What are some acute toxicities of anti cancer drugs?

A
  • due to inhibition of cell division

- tissue with fast renewal affected: bone marrow, GI mucosa cells, skin/hair

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9
Q

What are some delayed toxicities of anti cancer drugs?

A
  • infertility
  • secondary malignancies
  • anthracyclines can cause cardiac toxicity
  • methotrexate can cause pneumonitis
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10
Q

What are the two groups of alkylating agents?

A
  • Nitrogen mustards e.g. cyclophosphamide, ifosfamide

- Platinum analogues e.g. cisplatin, carboplatin and oxaliplatin

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11
Q

What is cyclophosphamide?

A

A prodrug -> must be activated in the liver to active metabolites

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12
Q

What are the indications of cyclophosphamide?

A
  • lymphoma
  • breast cancer
  • bone marrow transplants
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13
Q

What are some toxicities of cyclophosphamide?

A
  • myelosuppression
  • cardiac dysfunction in high doses
  • N&V
  • hemorrhagic cystitis (esp with high dose/long term therapy)
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14
Q

What is ifosfamide?

A

Analogue of cyclophosphamide, activated in the liver by CYP3A4

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15
Q

What is the MOA of ifosfamide?

A

inter- and intra-strand cross links in DNA causes cell death

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16
Q

Is ifosfamide cell cycle phase specific?

A

No. Cell cycle phase non specific.

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17
Q

What are the indications for ifosfamide?

A
  • testicular cancer

- diffuse large B-cell lymphoma

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18
Q

What is an administration instruction for ifosfamide?

A
  • must administer with mesna
  • vigorous hydration with normal saline pre and post administration
  • encourage pts to increase oral fluid intake
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19
Q

What are the toxicities of ifosfamide?

A
  • dose limiting toxicity is hemorrhagic cystitis
  • neurotoxicity (hallucinations, confusion etc)
  • N&V
  • nephrotoxicity
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20
Q

How to manage neurotoxicity of ifosfamide?

A
  • caution in elderly
  • caution in renal dysfunction
  • increase infusion time
  • avoid concurrent CNS drugs
  • decrease dose or discontinue with onset of symptoms
  • methylene blue as antidote
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21
Q

What is the indication of cisplatin?

A
  • solid tumours
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22
Q

What are the 5 toxicities of cisplatin?

A
  • Acute and delayed N&V (one of the most emetogenic drugs) (DOSE LIMITING)
  • cisplatin nephrotoxicity
  • ototoxicity (cannot hear high pitch sounds)
  • peripheral neuropathy
  • irritant to veins (phlebitis)
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23
Q

What is cisplatin induced nephrotoxicity?

A
  • deterioration of renal function and electrolyte wasting
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24
Q

How to manage cisplatin induced nephrotoxicity?

A
  • avoid in renal dysfunction
  • hydration with saline pre and concurrent with cisplatin, with potassium and magnesium supplementation
  • maintain urine output >100ml/h
  • provide mannitol and or furosemide for diuresis
  • prolong infusion time
  • amifostine as scavenger
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25
Q

What is carboplatin indicated for?

A

Solid tumours

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26
Q

What are the toxicities of carboplatin?

A
  • Myelosuppression (dose-limiting)

- Hypersensitivity

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27
Q

Advantages of carboplatin over cisplatin?

A
  • much lower incidence of nephrotoxicity, ototoxicity and delayed N&V than cisplatin
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28
Q

What is oxaliplatin indicated for?

A

Colorectal cancer

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29
Q

How do we administer oxaliplatin?

A

Stable only in D5W (dextrose)

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30
Q

What are the toxicities of oxaliplatin?

A
  • cumulative peripheral neuropathy
  • myelosuppression
  • nephrotoxicity (much less than cisplatin)
  • hypersensitivity
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31
Q

What are the enzyme inhibitors?

A

Topoisomerase I inhibitor: Irinotecan -> causes single stranded break

Topoisomerase II inhibitor: Etoposide, Anthracyclines (doxorubicin) -> causes double stranded break

32
Q

What is the active metabolite of irinotecan?

A

SN-38 is an active metabolite

33
Q

Is irinotecan cell cycle phase specific?

A

It is S phase specific.

34
Q

What is irinotecan indicated for?

A

Metastatic colorectal cancer

35
Q

What are the toxicities of irinotecan?

A
  • diarrhoea (dose-limiting) - both early and late diarrhoea -> treat with loperamide
  • cholinergic syndrome can occur (salivation, sweating, lacrimation, urination and diarrhoea) -> routinely premedicate with IV or SC atropine
36
Q

What is problematic about irinotecan?

A

UGT1A1 deficiency can cause SN-38 to accumulate

Hence, dose adjust.

37
Q

What is etoposide indicated for?

A

Solid tumours

38
Q

What are the toxicities of etoposide?

A
  • myelosuppression (primarily neutropenia)

- hypotension if infused too quickly

39
Q

What are the toxicities of anthracyclines?

A
  • dose limiting myelosuppression (primarily neutropenia)
  • cardiotoxicity (need baseline MUGA/ECHO)
  • alopecia
  • acute N&V
  • vesicant -> extravasation
  • red discolouration of urine
40
Q

How to prevent anthracycline-induced cardiotoxicity?

A
  • limit cumulative dose
  • fractionate doses
  • prolonged infusion
41
Q

What are the agents under the “antimetabolites” class?

A
  • methotrexate

- pyrimidine analogues

42
Q

MOA of antimetabolites?

A
  • structurally similar to naturally occurring compounds
43
Q

What are the toxicities of methotrexate?

A
  • dose limiting myelosuppression
  • mucositis, diarrhoea
  • pulmonary pneumonitis
44
Q

What drugs should be avoided when taking methotrexate?

A

Drugs that interfere with methotrexate excretion (renal excretion) eg NSAIDs, penicillin

45
Q

MOA of methotrexate?

A

Inhibits dihydrofolate reductase -> inhibits conversion of folic acid to tetrahydrofolate (active form of folic acid required for purine and thymidylate synthesis)

46
Q

What does high dose methotrexate require?

A

Therapeutic drug monitoring and folinic acid rescue

47
Q

Does methotrexate escape into third spaces?

A

Yes. Those w/ ascites or pleural effusions are at high risk for methotrexate toxicity.

48
Q

What are the pyrimidine analogues?

A

5FU and capecitabine

49
Q

MOA of 5FU?

A

Analog of pyrimidine uracil -> acts as pyrimidine antagonist

50
Q

What happens to 5FU in DPD deficiency?

A

5FU is degraded in the liver by DPD.

Hence, DPD deficiency -> toxicity

51
Q

What is the toxicity of 5FU?

A

Bolus - dose limiting myelosuppression

Continuous infusion - dose limiting hand-foot syndrome and diarrhoea

52
Q

What are the indications of capecitabine?

A

Colorectal and breast cancer

53
Q

MOA of capecitabine?

A

Orally active prodrug of FU, selectively activated by tumour cells

54
Q

How to administer capecitabine?

A

Give within 30 mins after a meal

55
Q

Toxicities of capecitabine?

A
  • hand-foot syndrome

- mucositis and diarrhoea

56
Q

What are the two groups of anti microtubules?

A
  • taxanes

- vinca alkaloids

57
Q

MOA of vinca alkaloids?

A

binds to tubulin and inhibits its polymerization

58
Q

What are examples of vinca alkaloids?

A
  • vincristine
  • vinblastine
  • vinorelbine
59
Q

In which phase of the cell cycle does vinca alkaloids act at?

A

Mitosis (metaphase)

60
Q

What are some toxicities of vincristine?

A
  • peripheral neuropathy

- ileus, constipation

61
Q

What are some toxicities of vinblastine and vinorelbine?

A
  • dose limiting neutropenia and thrombocytopenia

- neurologic toxicity and constipation can also occur but much less than vincristine

62
Q

MOA of taxanes?

A

Stabilize against depolymerization -> cannot recycle materials

63
Q

What are the pre-medications required for paclitaxel?

A

To prevent hypersensitivity,

  • H1 blocker
  • H2 blocker
  • corticosteroids
64
Q

What are the premeds required for docetaxel?

A

To prevent edema,

dexamethasone starting on the day before chemo

65
Q

What is tamoxifen?

A
  • selective estrogen receptor modulator
  • blocks estrogen from stimulating breast cancer cells
  • treatment of estrogen receptor positive breast cancer in premenopausal and post menopausal women
  • increases the risk of endometrial cancer and thromboembolic events in women treated with this drug
66
Q

What is letrozole (aromatase inhibitor)?

A
  • indicated for treatment of estrogen receptor positive breast cancer in post-menopausal women
  • reversible competitive inhibitor of enzyme aromatase
  • causes bone-related adverse effects eg bone pain, fractures and new onset osteoporosis -> supplement with calcium and vit D
67
Q

What are targeted cancer therapies?

A
  • drugs that interfere with specific molecules involved in cancer growth and survival
  • often cytostatic, whereas standard chemo drugs are cytotoxic
  • not necessarily have lesser side effects/drug interactions than standard chemo drugs
68
Q

What are examples of targeted cancer therapies?

A
  • tyrosine kinase inhibitors (TKI)

- VEGFR inhibitors

69
Q

What are examples of epidermal growth factor receptor TKI?

A

erlotinib, gefitinib, afatinib

70
Q

What are some toxicities of EGFR TKI?

A
  • dermatological toxicities

- diarrhoea

71
Q

What is the toxicity of rituximab?

A
  • infusion related reactions -> premedicate with paracetamol and diphenhydramine, start infusion slow and increase rate over time
72
Q

What is bevacizumab?

A
  • vascular endothelial growth factor inhibitor
  • used in colorectal cancer, lung cancer and kidney cancer
  • no premedications required
  • avoid in pts at high risk of bleeds or CNS metastasis
  • causes proteinuria: monitor urine protein, discontinue in nephrotic syndrome
73
Q

What is trastuzumab?

A

HER2 receptor antagonist

  • used in breast and gastric cancer
  • can cause cardiotoxicity
74
Q

What is the difference between passive and active immunotherapy?

A

Passive - Act on the tumour

Active - Act on immune system

75
Q

What is PD-1 and PD-L1?

A

PD-1 is the receptor found on T cells

PD-L1 is the ligand for the receptor.

76
Q

What is pembrolizumab and nivolumab?

A

PD-1 inhibitor

77
Q

What are the adverse effects of immunotherapies?

A

Immune-related adverse events - inflammation. Over-stimulated immune response. Can affect any tissue or organ in the body.

Manage using immunosuppresants like steroids.

Pharmacotherapeutics IV CA3 (4 decks)

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