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[AMS] 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

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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5
Q

How can one classify tumours according to chemosensitivity?

A
  • High sensitivity
  • Modest sensitivity
  • Low sensitivity
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6
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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7
Q

Identify five types of modest sensitivity tumours

A
  • Breast tumours
  • Colorectal tumours
  • Bladder tumours
  • Ovary tumours
  • Cervix tumours
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8
Q

Identify four types of low sensitivity tumours

A
  • Prostate tumours
  • Renal cell tumours
  • Brain tumours
  • Endometrial tumours
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9
Q

Identify the four groups of chemotherapy

A
  • Antimetabolites
  • Antibiotics
  • Alkylating/Platinating agents
  • Mitotic spindle inhibitors
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10
Q

Provide two examples of alkylating/platinating agents

A
  • Platinating – Cisplatin
  • Alkylating – nitrogen mustards e.g. Chlorambucil
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11
Q

Describe the mechanism of action of alkylating/platinating agents

A
  • Target DNA synthesis in G1/S phase
  • Forms covalent bonds with DNA nucleosides disrupting structure and preventing replication
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12
Q

Identify some specific ADRs of alkylating/platinating agents

A
  • Peripheral, sensory and motor neuropathy
  • High frequency ototoxicity
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13
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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14
Q

Provide some examples of microtubule poisons

A
  • Vinca Alkaloids
  • Taxanes
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15
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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16
Q

How do microtubule-binding agents affect microtubule dynamics?

A
  • Inhibit polymerisation
  • Stimulate polymerisation and prevent depolymerisation
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17
Q

Identify the specific ADR of microtubule poisons

A

Neurotoxicity: glove and stocking peripheral neuropathy

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18
Q

Provide an example of a glycopeptide antibiotic

A

Bleomycin

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19
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
20
Q

Identify the specific ADR of glycopeptide antibiotics

A

Pulmonary Fibrosis (10%)

21
Q

Provide an example of an anthracycline antibiotic

A

Doxorubicin

22
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
23
Q

Identify the specific ADR of anthracycline antibiotics

A

Cardiotoxic

24
Q

Provide two examples of antimetabolites

A
  • Methotrexate
  • 5-Fluorouracil
25
What is the mechanism of action of methotrexate?
Methotrexate inhibits **dihydrofolate reductase**, preventing DNA synthesis
26
What is Tamoxifen?
**Tamoxifen** is a SERM (selective oestrogen receptor modulator) and acts as antagonist of the oestrogen receptor in breast tissue
27
Describe the metabolism of Tamoxifen
Tamoxifen is a **prodrug** and is metabolised by **liver** to its active form which can competitively bind to oestrogen receptors
28
Describe the mechanism of action of Tamoxifen
Tamoxifen causes cells to remain in the G0 and G1 phase of the cell cycle
29
When can Tamoxifen therapy be used?
To be eligible for therapy those with breast cancer must be **ER (oestrogen receptor) positive**
30
Identify some common side effects of Tamoxifen treatment
- Hot flushes/sweats - Increased DVT/PE risk - Weight gain - Increased risk of endometrial cancer
31
What is the predicted response to chemotherapy dependent on?
- Performance score - Clinical stage - Prognostic factors/score - Molecular / cytogenetic markers
32
What are the different routes of administration for chemotherapy?
- **IV** - **PO** - **SC** (community setting) - **Into a body cavity** (bladder, pleural effusion) - **Intralesional** - **Intrathecal** (lumbar puncture / omaya reservoir – directly into ventricles) - **Topical** - **IM** (rarely)
33
Identify some common side effects of chemotherapy
34
Explain how acute renal failure occurs as a side effect of chemotherapy
**Acute renal failure** – hyperuricaemia caused by rapid tumour lysis leads to precipitation of urate crystals in renal tubules
35
Vomiting is multifactorial but includes direct action of chemotherapy drugs on the central chemoreceptor trigger zone. What are the different patterns of emesis?
- Acute phase (4 - 12 hours) - Delayed onset (2 - 5 days later) - Chronic phase (persist up to 14 days)
36
Mucositis is due to GI tract epithelial damage. Where does it commonly occur?
- May be profound and involve **whole tract** - Commonly worst in **oropharynx**
37
Mucositis is due to GI tract epithelial damage. How does this present?
- Sore mouth/throat - Diarrhoea - G.I. bleed
38
What causes variability in the pharmacokinetics of chemotherapy?
- Abnormalities in absorption - Abnormalities in distribution - Abnormalities in elimination - Abnormalities in protein binding
39
What is the result of the abnormalities in absorption?
- Nausea - Vomiting - Compliance - Gut problems
40
What is the result of the abnormalities in distribution?
- Weight loss - Reduced body fat - Ascites
41
What is the result of the abnormalities in elimination?
- Liver dysfunction - Renal dysfunction - Other medication
42
What is the result of the abnormalities in protein binding?
- Low albumin - Other drugs
43
Other drugs may increase plasma levels of the chemotherapy drug. What are the important drug reactions that should be considered during chemotherapy?
- Vincristine and **itraconazole** (common antifungal) - Capecitabine (oral 5FU) and **warfarin** - Methotrexate and **penicillin, NSAIDs** - Capecitabine and **grapefruit juice**
44
Which three factors should be monitored during chemotherapy treatment
- **Response of cancer** – radiological imaging, tumour marker blood tests, bone marrow/cytogenetics - **Drug levels** - **Organ damage** – creatinine clearance, echocardiogram
45
What principles can one learn from the fractional kill hypothesis?
- Bone marrow cells recover quicker than tumour cells - Hence a new dose of chemotherapy is given after bone marrow regeneration has occurred
46
Provide two examples of vinca alkaloids
- Vincristine - Vinblastine

[AMS] Clinical Pharmacology & Therapeutics (29 decks)

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