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Oncology > Principles of anti-cancer drug therapy > Flashcards

Principles of anti-cancer drug therapy Flashcards

1
Q

what is chemotherapy?

A

Chemotherapy usually refers to treatment
of cancer with drugs
Many of the drugs are cytotoxic
Interfere with cell growth or cell division
Action is not specific to cancer cells

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2
Q

Veterinary vs human chemotherapy

A 
Same drugs but smaller doses 
Less intense schedules 
palliation /control rather than cure 
Lack of intensive facilities 
Aim to prolong life, but QoL is paramount
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3
Q

chemo-sensitive tumours

A

Lymphoma
Leukaemias, myeloma
Disseminated MCT
Disseminated histiocytic sarcoma

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4
Q

highly metastatic tumours

A 
need adjuvant treatment post-op
OSA (osteosarcoma)
HSA (haemangiosarcoma)
high grade STS 
grade III MCT or grade II MCT with high mitotic index
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5
Q

contra-indication of using chemo

A

Shouldn’t be used when surgery or radiation

is a more effective alternative

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6
Q

administration routes

A 
Oral 
IV 
SC 
Intra-cavitary 
Intra-lesional
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7
Q

how do cyto-toxic drugs work

A

Cytotoxic drugs interfere with cell growth or division
Some act at specific stages of the cell cycle
Some are cell cycle non-specific
Most drugs work best on actively dividing cells…
tumours with a high mitotic index are more likely to be sensitive
Cells in G0 (resting) are relatively resistant

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8
Q

timing of treatment

A

Treat as early as possible in the disease course

Following surgery - Start treatment as soon as the surgical wound has healed

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9
Q

cell kill hypothesis

A

Tumour cell kill follows first order kinetics

A given dose of drug kills a fixed percentage of cells, as opposed to a fixed number of cells

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10
Q

dosing of cytotoxic drugs

A

Use at the maximum tolerated
dose - highest fractional kill with each treatment
avoid adverse effects
Multiple doses are required
Pulse dosing at intervals – Allow normal tissues to recover between doses but don’t allow tumour to regrow

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11
Q

combination chemotherapy

A

More likely to be effective than single agent – less selection pressure
Use drugs which:
1) Are known to be effective as single agent
2) Have different modes of action and don’t
interfere with each other
3) Act at different stages of the cell cycle
4) Don’t have overlapping toxicities

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12
Q

stages of chemo - induction

A

Initial treatment protocol, fairly intense

Aim to induce remission (i.e. state where tumour is not clinically detectable)

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13
Q

stages of chemo - maintenance

A

only in some protocols
Follows induction, less intense
Aim to maintain remission

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14
Q

stages of chemo - re-induction

A

When tumour relapses

Return to initial protocol - Aim to re-induce remission

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15
Q

stages of chemo - rescue

A

When tumour becomes resistant to current therapy

Use different drugs that tumour has not been exposed to before with different mechanism of action

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16
Q

dosing of chemotherapy agents

A

Cytotoxic drugs are usually dosed at MTD
Drugs are often dosed on a mg/m2 basis
Conversion charts e.g. BSAVA formulary
Small dogs <10 kg and cats are sometimes dosed on a mg/kg basis (e.g. doxorubicin)

17
Q

Metronomic therapy / RTKIs

A

Metronomic therapy inhibits angiogenesis; immunomodulatory
RTKIs interfere with cell signalling, angiogenesis /survival
Given on a continuous / semi-continuous basis
Responses are slower and less dramatic than conventional cytotoxic therapy
Stable disease or preventing progression may be a satisfactory response

18
Q

Factors affecting the success of chemotherapy - Tumour cell type

A

Intrinsic resistance e.g. many carcinomas, melanoma

19
Q

Factors affecting the success of chemotherapy - drug distribution

A

Blood supply

Barriers to diffusion

20
Q

Factors affecting the success of chemotherapy - development of resistance

A

Tumours are genetically unstable

Drugs - selection of resistant cell types

21
Q

myelosuppresion

A 
Neutropenia 
Thrombocytopenia 
Neutrophil nadir (lowest level) often ~1 week after a dose of chemotherapy 
Platelet nadir ~ 10d post-Tx 
Assess the neutrophil nadir 
Assess counts before administering next dose of any myelosuppressive drug 
Antibiotics may be required
dose reduction may be required
22
Q

vomiting - treatment

A

Bland diet
Anti-emetics – Maropitant *, Metoclopramide, Ondansetron
Gut protectants – Ranitidine, sucralfate, Omeprazole

23
Q

diarrhoea - treatment

A

Bland diet
Metronidazole
IVFT if severe
Other symptomatic Tx – loperamide, sulphasalazine

24
Q

anorexia - treatment

A

Maropitant if nauseous
Appetite stimulants e.g. cyproheptadine, mirtazepine
Feeding tubes

25
Q

drug extravasation - prevention

A

Cleanly-placed catheter
Firmly taped in
Flush with saline

26
Q

drug extravasation - treatment

A

Try aspiration of drug
Vincristine – hot compresses, hyaluronidase
Doxorubicin – ice, dexrazoxane

27
Q

Metabolism and excretion of chemotherapy drugs

A

Liver
Kidney
Dose reduction if function is impaired
Some drugs are activated by the liver (e.g. cyclophosphamide) – unpredictable action with impaired function

28
Q

Alkylating agents - mechanism of action

A

Substitute alkyl side chains for H+ ions in the DNA molecule
Interfere with DNA replication and transcription
Not cell-cycle specific
e.g. Cyclophosphamide

29
Q

Mitotic spindle inhibitors - mechanism of action

A

Cell cycle specific (G2/M phase)
Bind to tubulin, interfere with mitotic spindle formation - metaphase arrest
e.g. Vincristine

30
Q

anti-metabolites - mechanism of action

A

Mimic normal substrates in DNA / RNA synthesis (inhibit enzymes or non-functional molecules)
Cell-cycle specific - S-phase
Cytosine arabinoside

31
Q

platinum compunds

A

Cross-link DNA strands

Cell cycle non-specific

32
Q

anti-tumour antibiotics - mechanism of action

A

Not cell-cycle specific
Inhibit topoisomerase II
Break and cross-link DNA strands
Doxorubicin  free radical formation

33
Q

NSAIDs - mechanism of action

A 
COX-2 inhibition 
Anti-angiogenic 
Promote apoptosis, 
Anti-inflammatory, analgesic 
Effects on stromal cells
34
Q

Prednisolone

A

not cytotoxic

causes apoptosis of lymphoid / mast cells

35
Q

L-asparaginase

A 
not cytotoxic
Enzyme which breaks down L-asparagine 
Neoplastic lymphoid cells are dependent on an external supply of L-asparagine 
Inhibits protein synthesis 
Lymphoma
36
Q

Receptor Tyrosine Kinase Inhibitors

A

Small molecules that interfere with down-stream
signalling from cell surface growth receptors
Masitinib and toceranib for MCT – Inhibit signalling through KIT (and other RTKs) by blocking ATP binding site in the kinase domain, 30-40% of MCT have mutated KIT

Oncology (5 decks)

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