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SA Clinical Pharmacology & Therapeutics > S7) Cancer Chemotherapy > Flashcards

S7) Cancer Chemotherapy Flashcards

1
Q

What is the aim of chemotherapy?

A

The aim of chemotherapy is to kill/prevent replication of tumour cells at a greater rate than normal healthy tissue

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2
Q

What is the role of chemotherapy?

A
  • Curative

OR

  • Palliative
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3
Q

When is chemotherapy usually given?

A
  • Given as an adjunct to surgery/radiotherapy

OR

  • Given in isolation
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4
Q

which phase of the cell cycle cannot be targeted in chemotherapy

A

G0 → when there is no proliferation

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5
Q

what is growth fraction

A

proportion of cells dividing at any given time, the higher the growth fraction the more cells you can target

→ tumours are heterogeneous (some cells proliferate, die or are dormant) so repeated cycles are required to eradicate remaining and re growing cells

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6
Q

What are the factors leading to increased tumour growth?

A
  • Increased growth fraction
  • Decreased duration of cell cycle
  • Decreased rate of cell loss
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7
Q

why do we give chemo in a pulse like form

A

overall the destruction of the tumour cells is far greater than bone marrow cells. The timing is so the tumour cells don’t have time to recover before each next dose but the bone marrow cells do

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8
Q

How can one classify tumours according to chemosensitivity?

A
  • High sensitivity
  • Modest sensitivity
  • Low sensitivity (have to use other modes of treatment)
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9
Q

Identify five types of high sensitivity tumours

A
  • Lymphomas
  • Germ cell tumours
  • Small cell lung tumours
  • Neuroblastoma
  • Wilm’s tumour
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10
Q

Identify five types of modest sensitivity tumours

A
  • Breast tumours
  • Colorectal tumours
  • Bladder tumours
  • Ovary tumours
  • Cervix tumours
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11
Q

Identify four types of low sensitivity tumours

A
  • Prostate tumours
  • Renal cell tumours
  • Brain tumours
  • Endometrial tumours
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12
Q

Identify the four groups of chemotherapy

A
  • Antimetabolites
  • Antibiotics
  • Alkylating/Platinating agents
  • Mitotic spindle inhibitors
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13
Q

Provide two examples of alkylating/platinating agents

A
  • Platinating – Cisplatin, oxaliplatin
  • Alkylating – nitrogen mustards e.g. Chlorambucil
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14
Q

Describe the mechanism of action of alkylating/platinating agents

A
  • Target DNA synthesis in G1/S phase
  • Forms inter and intrastrand adducts (covalent bonds) with DNA nucleosides disrupting structure and preventing replication and so they die
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15
Q

Identify some specific ADRs of alkylating/platinating agents

A
  • Peripheral, sensory and motor neuropathy
  • High frequency ototoxicity
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16
Q

Describe the three possible mechanisms of resistance to alkylating agents

A
  • Decreased entry or increased exit of agent
  • Inactivation of agent in cell
  • Enhanced repair of DNA lesions produced by alkylation
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17
Q

name two anti-metabolites

A

5-fluorouracil: inhibits pyrimidine synthesis via inhibiton of thymidylate synthase

Metrotrexate: inhibits purine synthesis via inhibition of dihydrofolate reductase

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18
Q

Provide some examples of microtubule poisons

A
  • Vinca Alkaloids
  • Taxanes
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19
Q

Describe the mechanism of action of microtubule poisons

A
  • Target tubulin proteins in the mitotic phase
  • Chromosomes can’t align and separate into two daughter cells in synchrony
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20
Q

How do microtubule-binding agents affect microtubule dynamics?

A
  • Inhibit polymerisation: Vinca Alkaloids
  • Stimulate polymerisation and prevent depolymerisation: Texanes
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21
Q

how can cancer cells become resistant to some chemo drugs

A

→ body has its own repair system

→ cell cytoplasm has a P glycoprotein, these recognise foreign substances inside the cell and pump it out the cell

→ chemo drug is seen as foreign and can be pumped out cell

→ agents inside the cell (glutathione) is within the cytoplasm to mop up foreign material

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22
Q

Identify the specific ADR of microtubule poisons

A

Neurotoxicity: glove and stocking peripheral neuropathy

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23
Q

Provide an example of a glycopeptide antibiotic

A

Bleomycin

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24
Q

Describe the mechanism of action of glycopeptide antibiotics

A

Most effective in G2 stage:

  • Forms free radicals when chelated with Fe2+ which attack phosphodiester bonds in DNA
  • Results in cutting (scission) of DNA strands
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25
Q

Identify the specific ADR of glycopeptide antibiotics

A

Pulmonary Fibrosis (10%)

26
Q

Provide an example of an anthracycline antibiotic

A

Doxorubicin

27
Q

Describe the mechanism of action of anthracycline antibiotics

A

Targets DNA synthesis in “S” phase:

  • Intercalate between the base pairs in DNA which interferes with transcription/replication
  • Topoisomerase II inhibition
  • Generate free radicals – damage DNA
28
Q

Identify the specific ADR of anthracycline antibiotics

A

Cardiotoxic

29
Q

Provide two examples of antimetabolites

A
  • Methotrexate
  • 5-Fluorouracil
30
Q

What is the mechanism of action of methotrexate?

A

Methotrexate inhibits dihydrofolate reductase, preventing DNA synthesis

31
Q

What is Tamoxifen?

A

Tamoxifen is a SERM (selective oestrogen receptor modulator) and acts as antagonist of the oestrogen receptor in breast tissue

32
Q

Describe the metabolism of Tamoxifen

A

Tamoxifen is a prodrug and is metabolised by liver to its active form which can competitively bind to oestrogen receptors

33
Q

Describe the mechanism of action of Tamoxifen

A

Tamoxifen causes cells to remain in the G0 and G1 phase of the cell cycle

34
Q

When can Tamoxifen therapy be used?

A

To be eligible for therapy those with breast cancer must be ER (oestrogen receptor) positive

35
Q

Identify some common side effects of Tamoxifen treatment

A
  • Hot flushes/sweats
  • Increased DVT/PE risk
  • Weight gain
  • Increased risk of endometrial cancer → while it blocks oestrogen in the breast in the endometrium tamoxifen is a oestrogen agonist so increases the amount of oestrogen in uterus
36
Q

What is the predicted response to chemotherapy dependent on?

A
  • Performance score
  • Clinical stage
  • Prognostic factors/score
  • Molecular / cytogenetic markers
37
Q

What are the different routes of administration for chemotherapy?

A
  • IV
  • PO
  • SC (community setting)
  • Into a body cavity (bladder, pleural effusion)
  • Intralesional
  • Intrathecal (lumbar puncture / omaya reservoir – directly into ventricles)
  • Topical
  • IM (rarely)
38
Q

Identify some common side effects of chemotherapy

A

affects areas of the body that are fast replicating

39
Q

what is a common side effect of the chemo drug bleomycin

A

pulmonary fibrosis

40
Q

alopecia

A

→ hair thins 2-3 weeks

→ minimal with platinums

→ can wear scalp cooling hats to minimise hair loss

41
Q

what are some skin side effects of chemo drugs

A

Local:
→ irritation and thrombophlebitis of veins, extravasation

  • bleomycin (drug): hyperkeratosis, hyperpigmentation and pressure sores
  • hyperpigmentation
42
Q

Explain how acute renal failure occurs as a side effect of chemotherapy

A

Acute renal failure – hyperuricaemia caused by rapid tumour lysis leads to precipitation of urate crystals in renal tubules

→ cell break down releases cytokines that can cause crystals in the blood and block kidneys = rapid tumour lysis syndrome

43
Q

risks of chemo meds on GI tract

A

→ perforation at the site of the tumour = bad so need artificial feeding

44
Q

why does vomiting occur in chemo

A

→ triggers chemoreceptors in Brain and trigger them

45
Q

Vomiting is multifactorial but includes direct action of chemotherapy drugs on the central chemoreceptor trigger zone.

What are the different patterns of emesis?

A
  • Acute phase (4 - 12 hours)
  • Delayed onset (2 - 5 days later)
  • Chronic phase (persist up to 14 days)
46
Q

Mucositis is due to GI tract epithelial damage.

Where does it commonly occur?

A
  • May be profound and involve whole tract
  • Commonly worst in oropharynx
47
Q

Mucositis is due to GI tract epithelial damage.

How does this present?

A
  • Sore mouth/throat
  • Diarrhoea
  • G.I. bleed
48
Q

What causes variability in the pharmacokinetics of chemotherapy?

A
  • Abnormalities in absorption
  • Abnormalities in distribution
  • Abnormalities in elimination
  • Abnormalities in protein binding
49
Q

What is the result of the abnormalities in absorption?

A
  • Nausea
  • Vomiting
  • Compliance
  • Gut problems
50
Q

What is the result of the abnormalities in distribution?

A
  • Weight loss
  • Reduced body fat
  • Ascites
51
Q

What is the result of the abnormalities in elimination?

A
  • Liver dysfunction
  • Renal dysfunction
  • Other medication
52
Q

What is the result of the abnormalities in protein binding?

A
  • Low albumin
  • Other drugs
53
Q

Other drugs may increase plasma levels of the chemotherapy drug.

What are the important drug reactions that should be considered during chemotherapy?

A
  • Vincristine and itraconazole (common antifungal)
  • Capecitabine (oral 5FU) and warfarin
  • Methotrexate and penicillin, NSAIDs
  • Capecitabine and grapefruit juice
54
Q

Which three factors should be monitored during chemotherapy treatment

A
  • Response of cancer – radiological imaging, tumour marker blood tests, bone marrow/cytogenetics
  • Drug levels
  • Organ damage – creatinine clearance, echocardiogram
55
Q

What principles can one learn from the fractional kill hypothesis?

A
  • Bone marrow cells recover quicker than tumour cells
  • Hence a new dose of chemotherapy is given after bone marrow regeneration has occurred
56
Q

Provide two examples of vinca alkaloids

A
  • Vincristine
  • Vinblastine
57
Q

name two anti-metabolites

A

5-fluorouracil: inhibits pyrimidine synthesis via inhibiton of thymidylate synthase

Metrotrexate: inhibits purine synthesis

58
Q

problems that arise with combination therapy

A

→ if both drugs have similar side effects then you have to lower both doses but then they will have less of a treatment effect

59
Q

what causes variability of different chemo drug

A
60
Q

what are some drug-drug interactions involved In chemo drugs

A
61
Q

What are some ways you can monitor chemo treatment

A

→ radiological imaging, tumour marking, bone marrow

→ measure drug levels (methotrexate) and folic acid residue

→ check for organ damage (heart: creatinine clearance and echo)

SA Clinical Pharmacology & Therapeutics (36 decks)

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