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PED3006 Carcinogenesis > Chemotherapy From A Clinical Perspective > Flashcards

Chemotherapy From A Clinical Perspective Flashcards

1
Q

What kills patients with cancer

A

Local complication of tumour
Systemic complications of cancer
Direct complications of the treatments
Metastasis

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2
Q

Why is stage 4 difficult to treat

A

Require systemic treatment e,g drug administered into blood
Targeted treatment would be unaffected

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3
Q

What are the 4 types of treatments that can be given to a patients with cancer

A

Surgery
Radiotherapy
Supportive therapy
Systemic therapy

Many receive multi-modality treatments

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4
Q

What is supportive therapy

A

Addressing immediate symptoms e.g pain, emesis and phsycological issues

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5
Q

When is surgery beneficial

A

When the tumour is localised or at an early stage

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6
Q

When can radiotherapy be used

A

Can be used instead of surgery for localised cancers
Shrinks area of cancer to reduce burden

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7
Q

What are the 4 types of systemic cancer therapies

A

Chemotherapy
Hormone therapy
Immunotherapy
Targeted agents

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8
Q

Desiree chemotherapy

A

Targets DNA replication
Are anti-proliferative agents
Non-selective = normal tissue toxicity

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9
Q

What makes an effective chemotherapy drug

A

Reaches tumour cells
Sufficient [active component] enters cells
Tumour cells sensitive to drug
Normal tissue can recover/tolerate

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10
Q

What do you need to consider before combining treatments

A

Principles of tumour biology
Cellular kinetics
Pharmacology
Drug resistance

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11
Q

Describe combination treatment

A

Several different drugs each independently active against a disease

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12
Q

What is the result of combination therapy

A

Chance of emergence of drug resistance clone decreases
Rate of cell kill increases

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13
Q

Name a way that drugs in a combination treatment interact

A

Affect different phases of the cell cycle

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14
Q

Why should a patients fitness and co-morbidity be considered prior to combination treatment

A

Affect how well the body will tolerate the chemotherapy and the side effects

Allows to customise the dose for maximum efficacy and lowest toxicity

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15
Q

Why should organ functions be measured before any combined treatment

A

Kidney and liver metabolise drugs
-> low function = can’t metabolise or excrete the chemotherapy effectively

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16
Q

What are the 2 outcomes that we are trying to achieve in cancer treatment

A

Curative and non-curative intent

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17
Q

When is high dose/ radical chemotherapy used

A

Germ cell tumours e.g lymphomas and leukaemias

Completely get rid of the cancer in patients

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18
Q

What is neo-adjuvant chemotherapy

A

Course of chemo given before surgery/radiotherapy with the intent to cure the cancer

Used when a large tumour is localised and needs to be shrunk before surgery

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19
Q

When is palliative chemotherapy given

A

In the presence of advanced metastatic disease
Can’t cure it but can prolong survival

20
Q

What does the growth of tumour depend on

A

Actively growing fraction of the tumour

21
Q

What are the 3 classes of anti-tumour drugs that effect the mitotic cycle

A
  1. Cell cycle active - phase specific
  2. Cell cycle active - phase non-specific
  3. Non-cell cycle active
22
Q

What is the mechanism of action for bifunctional alkylating agents

A

Transfer an alkyl group to the N7 of guanine residue
= cross links with DNA
= no DNA synthesis + cell cycle arrest

23
Q

What phase of the cell cycle are bifunctional alkylating agents active in

A

All phases

24
Q

Name 2 alkylating agents

A

Cyclophosphamide

Melphalan

25
Q

What is the primary target of the folic acid analogue MTX

A

Dihydrofolate reductase

26
Q

How is folic acid transformed into tetrahydrofolate

A

Folic acid reduced -> dihydrofolate -> tetrahydrofolate via DHFR

27
Q

Describe thymidine synthesis

A

dUMP -> TMP via TS using 5,10-CH2THF

28
Q

Why is thymidine important

A

Without it = uracil disincorporation into DNA during replication
= double strand breaks during uracil excisions repair

29
Q

What state should folate be in order for thymidine synthesis to be happen

A

Reduced folate (dihydrofolate -> tetrahydrofolate)

30
Q

What is the mechanism of action of MTX

A

Inhibits dihydrofolate reductase

31
Q

How can normal tissue be rescued when folate levels droop during MTX treatment

A

Folinic acid rescue 24hrs after the end of NEMO

32
Q

Describe the mechanism of 5-Fluorouracil (5-FU)

A

Activated to FdUMP = inhibitor of TS acting at dUMP binding site

33
Q

Describe the mechanism of action of Pemetrexed

A

Multi-targeted anti-folate which inhibits: TS, DHFR and GARFT

34
Q

Describe the mechanism of action of Cisplatin

A

Covalently binds to DNA with preferential binding to the N7 position of guanine and adenine

Produces cross-links (intra/interstrand)

Adducts = inhibition of DNA synthesis and function

35
Q

How does Cisplatin affect the cell cycle

A

Arrest in G2 = accumulation of cells in G2/M

36
Q

How do you calculate the dose of carboplatin

A

Not by body surface but by Calvert formula

AUC x (GFR + 25)

37
Q

Describe the mechanism of action of Vinca Alkaloids

A

Inhibits tubulin polymerisation
Disrupts formation of microtubule assembly during mitosis
Arrests cell division

38
Q

What part of the cell cycle do vinca alkaloids affect

A

M-phase specific

39
Q

Describe the mechanism of action of Paclitaxel and Docetaxel

A

High affinity binding to microtubules
Stabilises tubulin polymerisation
= inhibition of mitosis and cell division

40
Q

Describe the difference between Topoisomerase I and II

A

I - causes single strand breaks and relieve torsion
II - causes DS breaks and allow other strand to pass and religate

41
Q

How do topoisomerase I inhibitors work

A

Directly binding to topoisomerase-DNA complex and prevent the re-ligation of DNA once its has been cut

42
Q

Name 2 topoisomerase I inhibitors

A

Irinotecan and topotecan

43
Q

Name a topoisomerase II inhibitor

A

Doxorubicin

44
Q

Describe the mechanism of action for topoisomerase II inhibitors

A

Forms a cleavable complex with DNA + topoisomerase II

45
Q

What are a few side effects of chemotherapy

A

Alopecia
Anaemia
Nausea and vomiting

PED3006 Carcinogenesis (9 decks)

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