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411 Oncology > L6 - Principles of systemic anticancer treatment > Flashcards

L6 - Principles of systemic anticancer treatment Flashcards

1
Q

What are the SIX possible approaches to cancer management?

A 
Surgery
Radiotherapy
Chemotherapy
Endocrine therapy
Targeted therapy
Immunotherapy
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2
Q

What are the main TWO goals when CURING cancer?

A

Destroy all cancer cells

Prevent recurrence

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3
Q

What are the main FOUR goals when CONTROLLING cancer?

A

Shrink tumour

Prevent tumour from growing & spreading further

Improve quality of life

Possibly prolong life

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4
Q

What are the main TWO goals when providing cancer PALLIATION?

A

Reduce & relieve cancer symptoms

Improve quality of life

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5
Q

What are the SEVEN types of chemotherapy/cytotoxic treatment?

A

Alkylating agents

Anthracyclines

Antimetabolites

Vinca alkaloids

Taxanes

Platinum compounds

Antibody-drug conjugates

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6
Q

What are the THREE types of non-cytotoxic treatment?

A

Endocrine therapy

Targeted therapy –> tyrosine kinase inhibitors

Immunotherapy –> monoclonal antibodies (checkpoint inhibitors)

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7
Q

What is adjuvant chemotherapy?

A

Given after surgery to reduce risk of relapse

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8
Q

What is neoadjuvant chemotherapy?

A

Given to shrink tumour enough to allow curative/less invasive surgery

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9
Q

What is palliative chemotherapy?

A

Given to relieve cancer symptoms, improve quality of life, possibly prolong life

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10
Q

When is chemotherapy most effective?

A

Proliferating cells, in M-phase (ie. when cells are dividing)

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11
Q

What are FIVE ways in which chemotherapy works?

A

Prevent cell replication

Inhibits synthesis of new DNA strands

Blocks formation of nucleotides necessary to create new DNA

Stops mitosis & cell division

Causes cell damage which leads to apoptosis

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12
Q

Why is chemotherapy typically given in 2/3 week cycles?

A

Timespan for neutrophils to come back up to safe levels for next chemotherapy cycle

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13
Q

What is chemotherapy dosing based on?

A

Body surface area (BSA)

BSA = square root [ (height cm x weight kg) / 3600 ]

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14
Q

When are dose modifications for chemotherapy doses (when calculated by BSA) needed?

A

Performance status, age, frailty

Kidney/liver function

Toxicity during cycles –> adjust dose for next cycle

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15
Q

Which cell cycle phase do taxanes work in?

A

M-phase (mitosis)

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16
Q

How do taxanes work?

A

Bind to microtubules & stabilise their structure

  • -> Prevent anaphase
  • -> Prevent cell division
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17
Q

What are examples of taxanes?

A

Docetaxel

Paclitaxel

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18
Q

What are examples of antimetabolites?

A

Cytarabine

Methotrexate

Gemcitabine

Fluorouracil (5FU)

Capecitabine

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19
Q

Which cell phase do antimetabolites work in?

A

S-phase (synthesis of DNA)

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20
Q

How do antimetabolites work? (general)

A

Substitute themselves for essential metabolites

–> Prevent DNA & RNA synthesis

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21
Q

What are examples of folate antagonists? (antimetabolites)

A

Methotrexate

Pemetrexed

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22
Q

How does methotrexate work? (antimetabolite)

A

Inhibits conversion of folic acid –> folinic acid by dihydrofolate reductase

Folinic acid needed for DNA replication

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23
Q

How does pemetrexed work? (antimetabolite)

A

Inhibits multiple enzymes involved in folate metabolism (inc. dihydrofolate reductase like methotrexate)

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24
Q

When is it preferred to give folic acid over folinic acid?

A

Smaller methotrexate doses

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25
Q

When is it preferred to give folinic acid over folic acid?

A

Larger methotrexate doses

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26
Q

Why is folinic acid important if methotrexate is being used?

A

Co-factor for DNA replication –> causes apoptosis when inhibited

If not supplemented following methotrexate administration, deficiency can cause mucositis, neutropenia etc.

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27
Q

How does fluorouracil (5FU) work? (antimetabolite)

A 
Pyrimidine analogue (actual nucleotide found in DNA)
--> "Fraudulent nucleotide" inhibits thymidylate synthetase, enzyme essential in DNA synthesis
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28
Q

What is the prodrug of fluorouracil (5FU)?

A

Capecitabine

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29
Q

How does folinic acid work with fluorouracil (5FU)?

A

Increases 5FU toxicity/efficacy –> stabilises complex with thymidylate synthetase

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30
Q

What are examples of anthracyclines?

A

Doxorubicin

Epirubicin

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31
Q

What cell phase do anthracyclines work in?

A

NON-phase specific

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32
Q

How do anthracyclines work?

A

Intercalation of base pairs in DNA double helix

  • -> Alkylation of DNA by free radicals
  • -> DNA strand breaks by inhibition of topoisomerase II (unwinding enzyme)
  • -> No transcription allowed
  • -> Inhibit DNA replication
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33
Q

What are examples of alkylating agents?

A

Cyclophosphamide

Ifosfamide

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34
Q

What cell phase do alkylating agents work in?

A

NON-phase specific

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35
Q

How do alkylating agents work?

A

Add alkyl groups to nucleic acids, proteins, amino acids, nucleotides

  • -> Crosslink DNA strands (“extra ladder rungs”)
  • -> Prevent strand separation & unwinding
  • -> Widespread cell damage –> apoptosis
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36
Q

What are examples of platinum compounds?

A

Cisplatin

Carboplatin

Oxaliplatin

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37
Q

What cell phase do platinum compounds work in?

A

NON-phase specific

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38
Q

How do platinum compounds work?

A

Add alkyl groups to nucleic acids, proteins, amino acids, nucleotides

  • -> Crosslink DNA strands (“extra ladder rungs”)
  • -> Prevent strand separation & unwinding
  • -> Widespread cell damage –> apoptosis
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39
Q

What cell phase do platinum compounds work in?

A

NON-phase specific

40
Q

Because cisplatin is highly emetogenic, nephrotoxic & ototoxic, what else needs to be given along with its administration?

A

Fluids –> lots to flush drug through while minimising adverse effects

Monitor

41
Q

Although carboplatin is more tolerable than cisplatin (less emesis/nephrotoxicity/ototoxicity), what does it have a higher risk of?

A

Myelosuppression (decreased bone marrow activity)
Neutropenia (low WBC)
Thrombocytopenia (low platelets)

42
Q

What formula is used to calculate carboplatin dosing?

A

Calvert formula –> based on CrCl, since carboplatin is almost exclusively excreted renally

43
Q

What is the main way of excretion of carboplatin

A

Renal excretion

44
Q

Which sort of cancer is oxaliplatin indicated for?

A

GI cancers. eg. colorectal

45
Q

Although oxaliplatin has the safest side profile compared to cisplatin & carboplatin, what does it have a higher risk of?

A

Cold-induced neuropathy
- Tingling etc. even when touching cold things, drinking cold drinks

Caution, esp. few days after chemo

46
Q

Adverse effects of chemotherapy are split into what phases?

A

Immediate

Early onset

Late onset

47
Q

What are TWO types of immediate adverse effects of chemotherapy?

A

Extravasation

Hypersensitivity reactions

48
Q

What are SEVEN types of early onset adverse effects of chemotherapy?

A

Haematological

Gastrointestinal –> mucositis, constipation, diarrhoea, nausea & vomiting

Dermatological –> eczema, psoriasis, SJS

Nephrotoxicity, hepatotoxicity

Myalgia (esp. with taxanes)

Neuropathy

Alopecia

49
Q

What are FIVE types of late onset adverse effects of chemotherapy?

A

Cardiac toxicity (esp. with anthracyclines)

Pulmonary toxicity

Neurotoxicity (esp. with vinca alkaloids)

Loss of fertility

Secondary malignancies –> most cytotoxic drugs are carcinogenic, since many cause DNA damage

50
Q

What is haematological toxicity? (early onset)

A

Most frequent toxicity –> may be dose-limiting

51
Q

What are the THREE types of haematological toxicity?

A

Neutropenia –> neutrophils
Thrombocytopenia –> platelets
Anaemia –> RBCs

52
Q

What is thrombocytopenia?

A

Low platelets

53
Q

What does thrombocytopenia result in?

A

Increased bleeding risk –> low platelets means clotting decreased

54
Q

How can thrombocytopenia be treated?

A

Platelet infusion

55
Q

What is anaemia?

A

Low haemoglobin in RBCs

56
Q

What are TWO common symptoms of anaemia?

A

Fatigue

Shortness of breath

57
Q

How can anaemia be treated?

A

RBC transfusion (epoetin alfa)

58
Q

Why is neutropenia most dangerous?

A

Occurs relatively quickly (short neutrophil lifespan)

Increased susceptibility to infection

May cause delay/dose reductions

59
Q

How can neutropenia (not febrile) be treated or prevented?

A

G-CSF

  • Filgrastim
  • Pegfilgrastim
60
Q

What is the difference between filgrastim & pegfilgrastim?

A

Pegylated version increases molecule size

  • -> Harder to metabolise/break down
  • -> Longer half-life & duration of action
  • -> Reduced dosing frequency

Filgrastim preferred in shorter chemo cycles eg. 1-2 weekly –> cleared fast enough for next dose
Pegfilgrastim required at least 14 days before next chemo cycle

61
Q

Why are G-CSF treatments not used in acute myeloid leukaemia?

A

Neutrophils come from the myeloid line –> in leukaemia, there are too many WBC.

G-CSF stimulates blood cell growth –> may increase risk of blood cancer

62
Q

What temperature is considered febrile neutropenia?

A

38.3°C & low neutrophil count < 0.5 x 10⁹/L

63
Q

How can febrile neutropenia be treated?

A

[guidelines]

Empiric antibiotics

G-CSF –> if no improvement after 48 hours

64
Q

What investigations are involved in a “septic screen”?

A

Blood cultures
Midstream urine sample
Chest xray

65
Q

What are the THREE phases of chemo-induced nausea & vomiting

A

Acute onset

Delayed onset

Anticipatory

66
Q

Which FOUR chemotherapy drugs have HIGH emetogenic risk?

A

Cisplatin

Dacarbazine

Anthracycline/cyclophosphamide combination

High-dose cyclophosphamide

67
Q

Which FOUR chemotherapy drugs have MODERATE emetogenic risk?

A

Carboplatin

Epirubicin

Irinotecan

Oxaliplatin

68
Q

Which FOUR chemotherapy drugs have LOW emetogenic risk?

A

Docetaxel

Paclitaxel

Fluorouracil

Methotrexate

69
Q

Which TWO chemotherapy drugs have MINIMAL emetogenic risk?

A

Vinorelbine

Vincristine

70
Q

What FOUR drugs are used for HIGH emetic risk with chemotherapy?

A

Aprepitant

Olanzapine –> dopamine receptors also targeted by antipsychotics

Dexamethasone

Ondansetron

71
Q

What TWO drugs are used for MODERATE emetic risk with chemotherapy?

A

Dexamethasone

Ondansetron

72
Q

What TWO drugs are used for LOW emetic risk with chemotherapy?

A

Dexamethasone

Ondansetron

73
Q

Which TWO types of emesis does dexamethasone work on?

A

Acute onset

Delayed onset

74
Q

Which TWO types of emesis does aprepitant work on?

A

Acute onset

Delayed onset

[only for highly emetic chemo]

75
Q

Which ONE type of emesis does ondansetron work on?

A

Acute onset

76
Q

Which TWO types of emesis does olanzapine work on?

A

Acute onset

Delayed onset

77
Q

Which ONE type of emesis does lorazepam work on?

A

Anticipatory –> helps calm patient down

Usually if have had bad experiences with chemo before –> psychological

78
Q

Which chemotherapy drugs usually cause diarrhoea?

A

Capecitabine

Irinotecan

Less commonly fluorouracil, docetaxel

79
Q

What is the THREE step treatment plan for chemotherapy-induced diarrhoea?

A

Loperamide (higher doses than normal)

Codeine

Octreotide (continuous SC infusion)

–> usually nil by mouth when on chemo –> total parenteral nutrition may be needed to reduce malnutrition

80
Q

How do monoclonal antibodies work? (TWO ways)

A

Stimulate patient’s immune system to destroy target

Prevent growth by blocking target

81
Q

What is the most common ADR with monoclonal antibodies?

A

Infusion-related –> allergic

82
Q

What are the THREE types of immune checkpoint inhibitors?

A

PD-1 inhibitors –> nivolumab, pembrolizumab

PD-L1 inhibitors –> atezolizumab

CTLA-4 inhibitors –> ipilimumab

83
Q

What does it mean when the Death Star is firing at Alderaan?

A

Tumour cells destroying normal cells. Activity not inhibited

84
Q

What does it mean when Admiral Ackbar is telling the Rebels about the Death Stars deflector shield?

A

Tumour cells have mechanisms to stop T cells from attacking them

85
Q

How does PD-1 & PD-L1 work?

A

PD-1 (T cell) usually binds to PD-L1 (normal cell) & this inactivates T cells –> do not attack

Tumour cells able to express PD-L1 –> T cell inactivated & tumour cell free to replicate/grow

86
Q

What does it mean with Han, Luke & Leia?

A

Deflectors shields need to be brought down by them on the forest moon of Endor

Checkpoint inhibitors

87
Q

How do checkpoint inhibitors work?

A

Block binding of PD-1 & PD-L1

  • -> T cell not inactivated by tumour cell
  • -> T cell can continue attacking tumour cells
88
Q

What does it mean when the Millenium Falcon destroys the Death Star’s exhaust port?

A

T cell attacking & destroying tumour cell

89
Q

What are the TWO main adverse effects of immunotherapy & TWO less common ones?

A

Immune-related adverse effects

Fatigue

Less common: nausea, low blood counts

90
Q

What are FIVE examples of immune-related adverse effects?

A

Hormonal effects –> eg. initial hyperthyroidism flare then persistent hypothyroidism

Hepatitis, nephritis

Pneumonitis –> breathlessness, cough

Colitis –> diarrhoea

Skin rash, itch

91
Q

What are the grades for immune-related adverse effects?

A

1: Mild
2: Moderate
3: Severe
4: Life-threatening

92
Q

How are the different grades of immune-related adverse effects managed?

A

1: Treat symptomatically; continue with checkpoint inhibitors
2: Withhold checkpoint inhibitor, start prednisone. Resume checkpoint inhibitor when symptoms return to grade 1

3 & 4: Permanently discontinue checkpoint inhibitor, start higher prednisone dose

If ADRs not resolved with prednisone, consider infliximab or mycophenolate (for hepatitis)

93
Q

How are other immune-related adverse effects (eg. hypothyroidism & hyperthyroidism) managed?

A

Hypothyroidism: levothyroxine

Hyperthyroidism: watch & wait –> generally initial flare followed by persistent hypothyroidism

94
Q

What does hypercalcaemia as a complication of cancer lead to?

A

Drowsiness

Confusion

Osteoporosis

Risk of cardiac arrhythmias

95
Q

How is hypercalcaemia as a complication managed?

A

Rehydration –> fluids

Zoledronic acid, pamidronate

96
Q

Why is zoledronic acid preferred over pamidronate for hypercalcaemia?

A

100x more potent

Less frequent administration

Shorter duration of infusions

411 Oncology (9 decks)

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