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Principles of Science > Principles of Clinical Oncology > Flashcards

Principles of Clinical Oncology Flashcards

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1
Q

What increases susceptibility to cancer?

A

Mutations in certain genes

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2
Q

What two ways can gene mutations occur?

A

Inherited

Acquired - random events, environmental insults

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3
Q

Give examples of four breeds of dog that are more susceptible to cancer

A

Boxers - lymhoma, MCT, others
Flat coat retrievers - soft tissue sarcomas
Irish wolfhound - osteosarcoma
GSD - haemangiosarcoma

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4
Q

Give examples of hormonal factors that can affect the aetiology of cancer

A

Oestrogen/progesterone in females - mammary tumours

Androgens in males - prostate carcinoma, perianal adenoma

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5
Q

What are the three environmental factors that affect the aetiology of cancer?

A

Exposure to carcinogens/mutagens
Exposure to mitogens
Exposure to biological agents

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6
Q

How does exposure to carcinogens/mutagens result in cancer?

A

Induce mutations in DNA - chemical agents (organic/inorganic). radionuclide, radiation

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7
Q

How does exposure to mitogens result in cancer?

A

Stimulates cell proliferation

Increased risk of random mutation

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8
Q

Why does UV radiation result in squamous cell carcinoma?

A

No pigment to soak up radiation

Causes mutations

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9
Q

What are some examples of biological agents that can result in cancer?

A

Retroviruses - FeLV
Poxviruses - BPV, equine sarcoids
Others - Helicobacter pylori, gastric carcinoma

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10
Q

What are proto-oncogenes?

A

Genes that normally: promote cell growth, promote proliferation, inhibit apoptosis

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11
Q

How can proto-oncogenes cause cancer?

A

Usually only activated during periods of tissue development or remodelling
Tightly controlled
Loss of control following mutation

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12
Q

What are two examples of tumour suppressor genes?

A 
p53
Retinoblastoma protein (Rb)
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13
Q

What do tumour suppressor genes normally do?

A

Prevent uncontrolled proliferation

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14
Q

What do tumour suppressor genes act like?

A

Brake pedal

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15
Q

What needs to occur for tumour suppressor function to be lost?

A

Both copies of the gene need to be mutated/deleted/silenced

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16
Q

What are the two types of mutation that can contribute to oncogenesis?

A

Gain of function mutations - oncogenes

Loss of function mutations - tumour suppressor genes

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17
Q

What two ways can genes be changed to contribute to oncogenesis?

A

Mutations - insertion, deletion, missense

Chromosomal reaarangements

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18
Q

What do chromosomal rearrangements induce?

A

Dysregulated gene expression

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19
Q

What must accumulate before a malignant cell can develop into a significant tumour?

A

Multiple mutations - usually around 10-12

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20
Q

How does a malignant cell progress into a tumour?

A

Cell proliferates
Only grows locally as can’t metastasize or ivade
Mutations inactivate DNA repair genes
More mutations accumulate, more genetic instability therefore more malignant potential
Malignant cells invade neighbouring tissues, enter blood vessels and metastasize to different sites

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21
Q

What are the ten hallmarks of cancer?

A 
Sustaining proliferative signalling
Evading growth suppressors
Activating invasion and metastasis
Enabling replicative immortality
Inducing angiogenesis
Resisting cell death
Deregulating cellular energetics
Avoiding immune destruction
Tour promoting inflammation
Genome instability and mutation
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22
Q

What is the traditional anti-cancer therapy method?

A

Poison the tumour more than you poison the host

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23
Q

What are the advantages of combination chemotherapy?

A

Attacks the cancer on several biological fronts at once
Reduces dose of each agent
Less adverse effects on healthy cells

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24
Q

How do cancer cells sustain proliferative signaling?

A

Become independent of host regulatory mechanisms

Become self sufficient

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25
Q

What are the three ways that a cancer cell becomes self sufficient?

A

Makes its own growth factors - act autocrine or paracrine
Alters receptors - activating mutations so receptor is constantly activated, receptor becomes overly expressed to respond to low ligand levels
Mutates signaling molecules - activating mutations switch on proliferation regardless of receptor activation

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26
Q

What is an example of a cancer where the receptors of the cell are altered?

A

MCT and KIT (stem cell factor receptor) mutations

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27
Q

What percent of canine MCT include KIT gene mutations?

A

30-50%

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28
Q

How does a KIT mutation cause uncontrolled proliferation?

A

Mutation in juxtamembrane region
Results in autophosphorylation
Cell signalling pathways acitvated
Cell survives and proliferates

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29
Q

What can be used to help treat MCT invloving these KIT mutations?

A

Receptor tyrosine kinase inhibitors

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30
Q

What is the difference between p53 and Rb, tumour suppressor molecules?

A

Rb - transduces growth inhibitory signals, determines whether cell cycle progression should proceed
p53 - receives iput from intracellular systems, halts cell cylce if viability is suboptimal, can trigger apoptosis

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31
Q

What breed has a germline p53 mutation and what does it predispose them to?

A

Bull Mastiffs

Predisposed to lymphoid neoplasia

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32
Q

What are the two major circuits that regulate cell death?

A

Extrinsic pathway - receives and processes extracellular death-inducing signals
Intrinsic pathway - senses and integrates a variety of signals of intracellular origin

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33
Q

What do both cell death pathways result in?

A

Activation of the Caspase cascade which executes apoptosis

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34
Q

How do cancer cells resist cell death?

A

Downregulate the death receptors

Up regulate members of the Bcl-2 family

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35
Q

What is cellular senescence primarily associated with?

A

Erosion of telomeres that protect the ends of chromosomes

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36
Q

How do cancer cells enable reproductive immortality?

A

Upregulate telomerase
Adds new telomeres`
Avoids apoptosis and senescence

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37
Q

Why must a cancer cell induce angiogenesis?

A

Reaches a size where it is at risk of hypoxia-induced cellular necrosis
Requires a dedicated blood supply to contiue growing

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38
Q

How do tumour cells induce angiogenesis?

A

Secrete angiogenic factors - VEGF
Acts on adjacent endothelial cells
Stimulates development of new blood vessels into the tumour

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39
Q

Why can receptor tyrosine kinase inhibitors help prevent angiogenesis induction?

A

VEGF is a receptor tyrosine kinase

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40
Q

How does invasion and metastasis of tumour cells usually begin?

A

Invade into nearby lymph or blood vessels

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41
Q

What can tumour cells do that can aid in invasion and metastasis?

A

Produce matrix metalloproteinases - disrupt surrounding tissues, allows invasion
Alter cell adhesino molecules - allows to detach and migrate

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42
Q

How do tumour cells reprogram energy metabolism?

A

Limit metabolism largely to glycolysis
Upregulate GLUT1 transporters
More efficient uptake of glucose into malignant cells

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43
Q

How can a tumour cell avoid immune destruction?

A 
Alters altered self antigens
Alters expression of MHC
Kill tumour infiltrating lymphocytes
Produce immunosuppressive mediators
Induce tolerance
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44
Q

How do tumour cells increase the rate of mutation?

A

Increase sensitivity to mutagenic agents

Breakdown one or several components of the genome maintenance machinery

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45
Q

Why is invasion of immune cells into a tumour counter-productive?

A

Enhance tumorigenesis as supplies: growth factors, imunosuppressive cytokines, angiogenic mediators

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46
Q

Why is the prevalence of cancer in pets increasing?

A

Pets are living longer - increased chance of developing cancer
Diagnostic techniques improving

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47
Q

Why is there a greater demand for cancer care in pets?

A

Owner awareness is increasing

May owners have a personal experience of cancer

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48
Q

How should pets with cancer be approached?

A 
Good communication vital
Positive yet realistic approach
Compassion
Well-informed advice to aid decision making
Seek help if out of your depth
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49
Q

What is the first step when presented with a patient with a mass lesion?

A

Decide if it is cancer or not

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50
Q

What are the differential diagnoses with a mass lesion?

A

Inflammatory lesions - abscess, granuloma
Haemoatoma
Seroma
Cyst

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51
Q

What is it important to do with a mass lesion?

A

Make a diagnosis

Don’t wait and see if it grows

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52
Q

What should be considered in history and physical examination when examining a mass lesion?

A 
How long has it been present?
Growth?
Any trauma?
Hot, red or painful?
Solid or fluid filled?
Well-defined or ill-defined?
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53
Q

What two samples can be taken of a mass lesion to assist diagnosis?

A

Cytology - fine needle aspiration

Histopathology - biopsy

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54
Q

What are the advantages of cytology in mass lesions?

A

Quick, cheap and easy
Distinguish inflammatory and neoplastic lesions
Gives information on cell type and morphology
Useful for analysis of effusions and bone marrow

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55
Q

How can inflammatory lesions be differentiated from neoplastic lesions on cytology?

A

Inflammatory - neutrophils, mixed cell poplation

Neoplastic - one cell type dominates

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56
Q

What does cell morphology help deterine with a ass lesion?

A

If it is benign or malignant

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57
Q

What does cytology not tell us about mass lesions?

A

Tissue architecture
Mitotic index
Invasion of vasculature/lymphatics
Tumour grade

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58
Q

What is the gold standard for diagnosis of mass lesions?

A

Histopathology

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59
Q

What does histopathology tell us about a mass lesion?

A 
Whether inflammatory or neoplastic
Cell type and morphology
Tissue architecture
Mitotic index
Invasion of vasculature/lymphatics
Degree of necrosis
Tumour grade
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60
Q

What should the next question be if a lesion is neoplastic?

A

What is the cell type/tissue of origin?

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61
Q

What are sometimes required to make/refine a diagnosis o cell type in a mass lesion?

A

Special stains

Immunohistochemistry

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62
Q

Why is a definitive diagnosis essential in mass lesions?

A

Different tumour types have different biological behaviour

Require different treatments

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63
Q

What are some features of malignancy in cells?

A

Increased N:C ratio
Abnormal mitotic figure
Hyperchromatic nucleus
Prominent nucleolus

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64
Q

What should be decided after cell/tissue of origin with a mass lesion?

A

Is it benign or malignant

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65
Q

Why is it important to decide whether a mass is benign or malignant?

A

Predict biological behaviour
Plan appropriate treatment
Advise the owner about the prognosis

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66
Q

What are the differences between a benign and malignant tumour?

A

Benign - grow slowly by expansion, dont invade surrounding tissues, dont invade lymph or vasculature, don’t metastasize, not life threatening, can often be cured
Malignant - grow more rapidly, invade and disrupt surrounding tissues, invade lymph and vasculature, metastasize to other parts o the body, treatment is more difficult, can be life threatening

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67
Q

What is tumour grade used to predict?

A

Behaviour of certain tumours - MCT, STS

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68
Q

What does the tumour grade depend on?

A 
Mitotic index
Degree of cellular differentiation
Invasion of surrounding tissues
Invasion of vasculature/lymphatics
Amount of necrosis
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69
Q

What are the three tumour grades?

A

Low grade
Intermediate grade
High grade

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70
Q

What are tumour grades important for?

A

Treatment planning
Prognosis
Communication when comparing outcomes

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71
Q

What system is used for mast cell tumours?

A

Patnaik grading systems - roman numerals for grade

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72
Q

What is the Kiupel system for gading MCTs?

A

Divides them into low grade and high grade

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73
Q

What should be assessed on histopathology if a tumour has been excised?

A

Margins

Ensure all tumour has been removed

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74
Q

What does clinical staging assess?

A

Extent of the disease in the patient

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75
Q

What does clinical cancer staging involve assessment of?

A

Primary tumour
Drainage lymph nodes
Distant metastatic disease

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76
Q

What is clinical staging important in?

A

Treatment planning
Prognosis
Communication

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77
Q

What system is often used for clinical staging?

A

TNM - primary tumour, node, distant metastasis

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78
Q

What is assessed for the T part of the TNM system?

A 
Size
Mobility
Ulceration
Relationship to surrounding tissues
Ulceration
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79
Q

What is assessed for the N part of the TNM system?

A

Drainage lymph nodes - size, mobility, relationship to surrounding tissues, texture, consistency

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80
Q

What is used for internal lymph node assessment?

A

Imaging

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81
Q

What is an FNA used to decide when clinically staging tumours?

A

Assess if lymph node metastasis is present or not

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82
Q

What is the M part of the TNM system usually assessed via?

A

Imaging - radiography, ultrasound, CT, MRI

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83
Q

What is the most common site for metastasis in small animals?

A

Lungs

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84
Q

What can give clues whether distant metastasis has occurred?

A

History and physical examination

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85
Q

Describe the 5 stages in the WHO system for staging lymphoma

A

Stage I - involvement limited to single node or lymphoid tissue in a single organ
Stage 2 - involvement of more than one lymph node in a regional area
Stage III - generalised lymph node involvement
Stage IV - liver and/or spleen involvement
Stage V - manifestation in the blood and involvement of bone marrow and/or other organ systems

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86
Q

What are the substages of the WHO system for staging lymphoma?

A

a - without systemic signs

b - with systemic signs

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87
Q

What are paraneoplastic syndromes?

A

Systemic effects of a tumour

Occur at a distant site to the tumour

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88
Q

What can cause paraneoplastic syndromes?

A

Secretions of: hormones, hormone like-substance enzyme
Cytokine production
Immune mediated mechanisms

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89
Q

What might concurrent illnesses affect in a cancer patient?

A

Treatment plan

Prognosis

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90
Q

What are the four baseline tests used to assess a cancer patient?

A

Haematology/CBC
Biochemistry
Urinalysis
Coagulation parameters (when indicated)

91
Q

Why is haematology essential prior to starting any chemotherapy?

A

Need for a baseline

Many chemotherapy drugs are myelosuppressive - affect ability to produce new blood cells

92
Q

What three things should be checked for on haematology?

A

Anaemia - common, occurs for many reasons
Cytopenias - might reflect myelophthsis or immune-mediated disease
Abnormal cells

93
Q

What is biochemistry used to assess in a cancer patient?

A

General health status

94
Q

What do we assess on a biochemistry in a cancer patient?

A

Organ damage/function

95
Q

Why do we need to assess organ damage/function in a cancer patient?

A

Drugs metabolised and excreted via liver and kidneys
Damage could affect choice and dose of drugs
Important prior to general anaesthetic and chemotherapy

96
Q

What else is it important to look for in a biochemistry of a cancer patient?

A

Paraneoplastic effects of the tumour

97
Q

What are three examples of paraneoplastic effects that can be seen on a biochemistry?

A

Hypercalcaemia - tumour production of PTH-rp, untreated will cause renal damage
Hypoglycaemia - insulin secretion, secretion of insulin-like growth factors
Hyperglobulinaemia - excessive antibody production

98
Q

What is urinalysis used for in a cancer patient?

A

Baseline screening for underlying renal problems

99
Q

When would you do a coagulation profile in a cancer patient?

A

If they have bleeding tendencies

100
Q

What abnormalities in coagulation can cancers cause?

A

Thrombocytopenia
Hypercoagulability
Hypocoagulability

101
Q

What might cancer patients present as instead of a mass presence?

A

Clinical signs relating to a paraneoplastic syndrome

102
Q

What are ten examples of paraneoplastic effects that a cancer patient may present with?

A 
Hypercalcaemia
Hypoglycaemia
Hyperviscosity
Gastric ulceration/vomiting
Endocrine problems
Pyrexia
Immune-mediated problems
Hypertrophic osteopathy
Dermatologic manifestations
Cancer cachexia
103
Q

What is essential when discussing cancer treatment with owners?

A

Good communication

104
Q

What should be covered when assessing owners expectations and goals?

A

Whether the cancer can be cured
Induction of remission for a time period
Is the aim to reduce tumour burden or control disease
Is treatment just palliative

105
Q

What must be maintained throughout cancer treatment?

A

Good quality of life

106
Q

What ethical and physiological issues need to be considered when discussing cancer treatment?

A

Owner’s personal experience with cancer
Concerns about complications/adverse effects - surgery has cosmetic appearance, chemotherapy lower doses in animals so less severe adverse effects, radiation has less intensive schedules than people but need general anaesthetic

107
Q

What nine things should be considered when discussing cancer treatment?

A 
Owner's expectations
Quality of life
Psychological factors
Patient temperament
Patient general health status
Possible complications
Time commitment/logistics
Cost
Prognosis
108
Q

What are seven cancer treatment options?

A 
Surgery
Radiation treatment
Chemotherapy
Molecular targeted drug therapy
Anti-angiogenic therapy
Immunotherapy
Others - photodynamic, electrochemotherapy etc.
109
Q

What are the most common options for cancer treatment?

A

Surgery
Radiation
Chemotherapy

110
Q

What is surgery the treatment of choice for with cancer?

A

Primary carcinomas
Sarcomas
Mast cell tumours

111
Q

What is radiation treatment the primary treatment for?

A

Nasal tumours

Localised, radiosensitive, non-resectable tumours

112
Q

What is radiation therapy frequently used as?

A

Adjunctive therapy - follow incomplete resection of other tumours
Neo-adjuvant surgery - shrink tumours prior to surgery

113
Q

What is chemotherapy indicated for in cancer patients?

A

Treatment of systemic disease - lymphoma, leukaemia, myeloma, systemic mast cell disease, disseminated histiocytic sarcoma

114
Q

What can chemotherapy be used for in highly metastatic cancers?

A

Adjunctive treatment

Used following surgical removal of the primary tumour

115
Q

What is essential when providing supportive care to a cancer patient?

A

Ensuring good quality of life

Anticipate and prevent adverse effects

116
Q

What six things should be considered when giving supportive care to a cancer patient?

A

Nutrition- monitor BCS/weight, ensure adequate intake
Dehydration - IVFT
GI problems - patients getting chemotherapy, consider gut protectants, anti-emetics or appetitie stimulants
Antibiotics - if neutropenic
Analgesia - short and long term, NSAIDs
Physiotherapy

117
Q

What can cytotoxic drugs interfere with?

A

Cell growth

Cell division

118
Q

What can chemotherapy drugs be?

A

Carcinogenic
Mutagenic
Teratogenic

119
Q

Who shouldn’t handle chemotherapy drugs or body fluids from chemotherapy patients?

A

Pregnant women

Children

120
Q

What should not be done with cancer tablets/capsules?

A

Crush or break tablets
Open capsules
Reformulated if necessary by special pharmacy

121
Q

What needs to be worn when administering cancer tablets?

A

Gloves

Wash hands afterwards

122
Q

What should cancer tablets be dispensed in?

A

Child-proof container
Clearly labelled as containing cytotoxic drugs
Blister packs into strips and put into childproof container

123
Q

What must be done with excess cytotoxic drugs?

A

Returned to practice

Destroyed by incineration

124
Q

What should injectable cytotoxic agents be drawn in?

A

Syringes in a cytotoxic safety cabinet

Phaseal equipment

125
Q

What should be worn when administering injectable cytotoxic drugs?

A

Protective clothing - chemotherapy gloves, waterproof long-sleeved gown, face mask and goggles

126
Q

Describe administering intravenous chemotherapy

A

Good restraint
Firmly tape catheter in place
Use designated, quiet area of the hospital with no through traffic
Luer-locking connections
Flush catheter before and after drug with 0.9% saline
Work over an absorbent pad

127
Q

Why must body waste/excreta of cancer patients be handled with care?

A

Small traces of drug may be present in the body waste for prolonged periods

128
Q

What are some sensible precautions when handling body waste/excreta from cancer patients?

A

Wearing gloves to clean up
Double bag faeces/cat litter/kennel waste
Designate toileting area if possible
Avoid contact with saliva

129
Q

What is the definition of neoplasia?

A

Uncontrolled proliferation of cells
Continues in absence of inciting cause
Neoplastic cells originate from a single cell which has undergone mutation and lost the ability to control its division

130
Q

What is fundamental to accurate diagnosis of neoplasia?

A

Good communication between the clinician and the pathologist

131
Q

What are the gross features of a benign tumour?

A 
Growth by expansion
Low to moderate growth rate
Well demarcated from surrounding tissue
Compresses surrounding tissue
Smooth in gross outline
Surrounding connective tissue capsule
Freely mobile on palpation
Homogenous cut surface
Little haemorrhage or necrosis
Surgical removal often easy
No recurrence if completely excised
No metastasis
132
Q

What are the microscopic features of benign tumours?

A 
Similar to tissue of origin
Well organised
Endocrine tumours can be functional producing hormones affecting other parts of the body
Surrounding connective tissue capsule
Doesn't broach the capsule
Few or no mitoses
Generally no haemorrhage or necrosis
133
Q

What are the gross features of malignant tumours?

A 
Growth by invasion
Not encapsulated
Not mobile on palpation
Complete removal often difficult
Often recurs after excision
Ulcerates if on skin or mucosal surface
Internal necrosis and haemorrhage
Can metastasise to local lymph nodes and lungs
134
Q

What are the microscopic features of malignant tumours?

A

Variable cell size and shape - pleomorphism
Variable nuclei size and shape - anisokaryosis
Increased N:C ratio
Prominent nucleoli
Presence of normal/abnormal mitoses
Loss of cohesiveness and structure
Malignant fusion leading to formation of multinucleated cells
Secondary changes - necrosis, fibrosis, inflammation
Not usually encapsulated

135
Q

What word describes a benign tumour of the surface epithelia?

A

Papilloma

136
Q

What word describes a benign tumour of glandular epithelia?

A

Adnemoa

137
Q

What is a malignant tumour of epithelial origin?

A

Carcinoma

138
Q

What are malignant tumours of glandular epithelia termed?

A

Adenocarcinoma

139
Q

What is a granuloma?

A

Organised type of chronic inflammation

140
Q

How do you describe tumours of mesenchymal origin

A

Benign add -oma to tissue of origin

Malignant add -sarcoma to tissue of origin

141
Q

What is a lymphoma?

A

Tumour of the lymphoid system

Usually malignant

142
Q

What is a melanoma?

A

Tumour of melanocytes

Can be benign or malignant

143
Q

What are leukaemias?

A

Tumours derived from the cells of the bone marrow which circulate in the blood

144
Q

What are teratomas?

A

Germ cell tumours with elements of ectoderm, endoderm and mesoderm

145
Q

What are sarcoids?

A

Low grade fibrosarcomas commonly seen in horse skin

146
Q

What are the four ways a tumour can metastasize?

A

Lymphatics - carcinoma
Vascular - sarcoma
Trans-cavity - mesothelioma
Local - multiple tumour types

147
Q

What are multicentric tumours?

A

Multiple tumours that present at first presentation

Difficult to determine primary site

148
Q

What are some examples of malignant tumours that metastasize rapidly and constantly?

A 
Tonsillar carcinomas
Pancreatic carcinomas
Osteosarcomas
Oral and digital melanomas
Mammary carcinomas - cats
149
Q

What are some examples of tumours that metastasise slowly or rarely?

A

Squamous cell carcinomas - invade extensively before metastasis
Fibrosarcomas - recur at site of excision

150
Q

What are some examples of things used in immunohistochemistry that can assist identification?

A

Cytokeratin - epithelial marker, carcinoma
Vimentin - mesenchymal marker, sarcoma
CD3 - T cell marker, T cell lymphoma
CD79a - B cell marker, B cell lymphoma

151
Q

What is tumour grading a measure of?

A

Differentiation

152
Q

What does not always correlate with tumour grade?

A

Prognosis

153
Q

What four ways are there of tumour grading?

A

Light microscopy
Immunophenotyping
Detection of genetic mutations
Use of proliferation markers

154
Q

Describe tumour grading using light microscropy

A

High grade - poorly differentiated

Low grade - well differentiated

155
Q

How does tumour grading on immunohistochemistry work?

A

Tumours become poorly differentiated - high grade

Lose expression of expected tissue markers

156
Q

What is standard practice for grading lymphomas in people?

A

Detection of specific mutations using cytogenetics

157
Q

What is valuable for mast cell tumour grading in dogs?

A

Detection of proliferation markers - Ki-67

158
Q

How can the pathologist help the clinician?

A 
Help obtain definitive diagnosis
Shortlist likely differential diagnoses
Estimate a prognosis
Formulate a treatment plan
Client education
Clinical audit
159
Q

What should you consider when choosing a pathologist?

A 
Service
Quality
Confidence
Cost
Location
160
Q

What should a biopsy report contain?

A 
Signalment and clinical history
Gross description
Clear concise histological description
Diagnosis or list of DDx
Comments on biological behaviour and prognosis
161
Q

What should a histological description from a pathologist include?

A

Cellular morphology
Mitotic index
Tissue or lymphatic invasion
Adequacy of surgical margins

162
Q

What are the three requirements the pathologist needs from the clinician?

A

Representative sample
Correctly submitted sample
Full clinical history

163
Q

Describe a representative sample

A 
Incisional or excisional biopsy
Include marign of normal tissue
Avoid necrotic and cavitated areas - not bone tumours need sample from that area
MNark margins of interest
Identify samples from different sites
164
Q

Describe a correctly submitted sample

A

Fix promptly in a large vlume of neutral buffered formalin
Intact tissue specimens should be no greater than 2cm
Larger specimens can be submitted unfixed if close to laboratory
Follow Royal Mail guidelines for sending specimens
Labels should be indelible
Names - practice, owner and animal
Sample site

165
Q

What is chemotherapy?

A

Treatment of cancer with cytotoxic drugs

166
Q

How do cytotoxic drugs work?

A

Interfere with cell growth or cell division
Target rapidly dividing cells
Not specific to cancer cells and can affect body’s normal rapidly dividing cells

167
Q

What is required with cytotoxic drugs?

A

A balance between efficacy and toxicity

168
Q

What are the major differences between veterinary and human chemotherapy?

A

Lower doses of drugs used in animals
Less intensive schedules in animals
Often trying to control disease than cure in animals
Lack of intensive facilities for management of complications in animals
Quality of life is still paramount

169
Q

For what six things is chemotherapy indicated?

A

Primary treatment for disseminated disease
Adjuvant therapy following surgery
Certain tumours following complete resection
Neo-adjuvant chemotherapy
Treatment of chemosensitive tumours where surgery or radiation is not possible
Primary treatment for transmissible veneral tumour

170
Q

When should chemotherapy not be used?

A

When surgery or radiation treatment is a more effective alternative

171
Q

What are the routes of administration for cytotoxic drugs?

A 
Oral
IV
Sub cutaneous
Intra-cavitary
Intra-lesional
172
Q

When is cytotoxic chemotherapy most likely to be effective?

A

When disease burden is low

173
Q

When is the best time to treat cancer with cytotoxic drugs?

A

Early in the disease course
If using as adjuvant let the wound heal first
With tumours with a high mitotic index

174
Q

What is the cell kill hypothesis?

A

Tumour cell kill follows first order kinetics

A dose of drug will kill a fixed percentage of the tumour population as opposed to a number of cells

175
Q

Describe cytotoxic drug dosing

A

Should be used at maximum tolerated dose
Multiple doses usually required
Pulse dosing often used

176
Q

What are the principles of combination chemotherapy?

A

Use drugs that: have been shown to be effective individually, have different modes of action and don’t interfere with each other, act at different stages of the cell cycle, don’t have overlapping toxicities

177
Q

What are most cytotoxic drugs dosed on?

A

mg/m2 basis

178
Q

What are the four stages of chemotherapy?

A

Induction - initial treatment protocol, fairly intense, aim to induce remission
Maintenance - only in some protocols, follows induction, less intense, aim to maintain remission
Re-induction - when tumour relapses, return to initial protocol, aim to re-induce remission
Rescue - when tumour becomes resistan to current therapy, use different drugs that tumour hasn’t been exposed to

179
Q

What are two alternatives to conventional cytotoxic chemotherapy?

A

Metronomic chemotherapy/continuous low dose chemotherapy

Receptor tyrosine kinase inhibitors

180
Q

What is the aim in metronomic chemotherapy?

A

Slow growth by inhibiting angiogenesis

Decrease circulating regulatory T-cells

181
Q

What are the effects of receptor tyrosine kinase inhibitors?

A

Inhibit angiogenesis
Reduce proliferation
Promote apoptosis

182
Q

What four factors affect the success of chemotherapy?

A

Tumour type - some highly sensitive, others resistant
Penetration of drug - depends on blood supply and natural barriers
Development of resistance - mutations occur creating resistance, drug exposure selects for resistance
Multi-drug resistance

183
Q

What are the four main adverse drug reactions to cytotoxic drugs?

A

Myelosuppression
GI toxicity
Poor hair growth/whisker loss
Drug extravasation

184
Q

What can myelosuppression by chemotherapy result in?

A

Neutropenia

Thrombocytopenia

185
Q

What is the dose limiting cytotoxic effect of many agents?

A

Neutropenia

186
Q

When is the lowest level of neutrophils often observed?

A

One week after chemotherapy dose

187
Q

What should be done to avoid myelosuppression?

A

Monitor CBC regularly in animals
Take CBC prior to each administration of myelosuppressive drug
Monitor neutrophil nadir
Reduce dose if low neutrophils or sepsis occurs

188
Q

What should be done if neutropenic and pyrexic/sick?

A

Give IV broad spectrum antibiotics

189
Q

What can occur with cytotoxic drugs in the GI tract?

A

Anorexia
Vomiting
Diarrhoea

190
Q

What can GI adverse effects have a major effect on?

A

Quality of life

191
Q

What should be done if GI AEs are experienced after drug administration?

A

Take prophylactic measures next time

192
Q

What should be done when vomiting is a GI AE?

A

Bland diet
Gut protectants
Anti-emetics

193
Q

What should be done if diarrhoea is a GI AE?

A

Bland diet

Metronidazole for immunomodulatory effects

194
Q

What shuold be done if anorexia is a GI AE?

A

Maropitant if nauseous
Appetite stimulants
Feeding tubes

195
Q

What can many IV chemotherapy drugs cause if extravasated?

A

Irritation

Blistering (vesication)

196
Q

What should be done if extravasation occurs?

A

Leave catheter in place
Withdraw as much drug as possible
Apply heat packs or ice
Seek specialist advice

197
Q

What toxicity effects does Doxorubicin have?

A

Cardiotoxicity in dogs - dysrhythmias during administration, chronic toxicity more significant, more likely to occur at cumulative doses
Mast cell degranulation - wheals, urticaria, pruritus, oedema, vomiting, diarrhoea, dyspnoea, hypovolaemic shock
Nephrotoxicity in cats
Vesicant if injected perivascularly

198
Q

How can Doxorubicin toxicity be prevented?

A

Administer over 20-30 minutes
Monitor shortening by echocardiography for contractilty decreases
Use with care in breeds predisposed to heart disease

199
Q

What toxicity effects does cyclophosphamide have?

A

Haemorrhagic cystitis in dogs - rare in cats

200
Q

How can cyclophosphamide toxicity be prevented?

A 
Allow free access to fresh water
Dose in the morning
Allow plenty of opportunity to go out
Divide dose over two days if high
Avoid prolonged courses of administration
Treatment difficult
201
Q

What toxicity effects does Vincristine have?

A

Peripheral neuropathies
Ileus/constipation in cats
Skin sloughs if injected perivascularly

202
Q

What toxicity effects does Lomustine have?

A

Hepatotoxicity - particularly dogs, monitor ALT prior to dose, consider SAMe
Nephrotoxicity - monitor USG, dipstick for glucosuria

203
Q

What toxicity effects do Platinum drugs have?

A

Nephrotoxicity
Cisplatin causes vomiting via CTZ - give antiemetics
Irritants if injected perivascularly

204
Q

What drugs should not be given to cats?

A

Cisplatin - fatal pulmonary oedema

5-FU - extreme neurotoxicity

205
Q

What do some herding breeds have an increased sensitivity to?

A

Vinca alkaloids

Doxorubicin

206
Q

How do alkylating agents work?

A

Substitute an alkyl group for H+ ion
Causes cross linkage and breaking of DNA
Interferes with DNA replication and transcription

207
Q

What are some examples of alkylating agents?

A 
Cyclophosphamide
Lomustine
Melphalan
Chlorambucil
Procarbazine
Dacarbazine
208
Q

How to mitotic spindle inhibitors work?

A

Bind to tubilin
Prevent normal assembly of microtubules
Cause mitosis to stop in metaphase
Only affects G2/M phase

209
Q

What are some examples of mitotic spindle inhibitors?

A

Vincristine
Vinblastine
Vinorelbine
Taxanes

210
Q

How do anti-metabolites work?

A

Mimic normal substrates in nucleic acid metabolism
Inhibit enzymes
Lead to production of non-functional molecules
Interfere with DNA synthesis
Specific to S phase

211
Q

What are some examples of anti-metabolites?

A 
Cytosine arabinoside/cytarabine
Methotrexate
Hydroxycarbamide
5-fluorouracil
Gemcitabine
Azathioprine
212
Q

How do anti-tumour antibiotics work?

A 
Prevent DNA and RNA synthesis
Inhibits topoisomerase II (untangles DNA strands)
Breaks DNA strands
Cross-links DNA
Free radical oxidative damage
213
Q

What are some examples of anti-tumour antibiotics?

A

Doxorubicin
Epirubicin
Mitoxantrone
Actinomycin-D

214
Q

How do platinum compounds work?

A

Similar to alkylating agents
Inter- and intrastrand crosslinks in DNA
Interferes with DNA synthesis and transcription

215
Q

What are some examples of platinum compounds?

A

Cisplatin

Carboplatin

216
Q

How do corticosteroids help fight cancer?

A

Cause apoptosis of lymphoid and mast cells

217
Q

What are two examples of cancer treating corticosteroids?

A

Prednisolone

Dexamethasone

218
Q

What are the adverse effects of corticosteroids?

A 
Polydipsia
Polyuria
Polyphagia
Excessive panting
Muscle weakness
Slow wound healing
Immunosuppression
219
Q

How does L-asparaginase work in cancer treatment?

A

Breaks down L-asparagine
Reduces amount present
Neoplastic lymphoid cells can’t synthesise
Extracellular supply diminished so die

220
Q

What is a possible side effect of L-asparaginase?

A

Allergic/anaphylacitc reaction

221
Q

How do NSAIDs help in cancer treatment?

A 
Thought to involve COX-2 inhibition
Inhibit angiogenesis
Promote apoptosis
Anti-inflammatory
Analgesic
222
Q

What are NSAIDs used in for cancer treatment?

A

Continuous low-dose chemotherapy protocols

Metronomic chemotherapy protocols

223
Q

How do receptor tyrosine kinase inhibitors work against cancer?

A

Interfere with cell signaling

Inhibit signaling through KIT receptors

Principles of Science (9 decks)

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