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oncology Flashcards

1
Q

what are oncogenes?

A

needed for normal growth and are tightly controlled but the control can be lose with mutation

can be expressed by some viruses

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2
Q

what are tumour supressor genes?

A

stop cells from proliferating out of control

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3
Q

how are tumour supressor genes function lost?

A

by both copies being mutated / deleted / silenced

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4
Q

how many mutations need to be acuumulated to initiate a tumour?

A

10-12

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5
Q

what are the 6 hallmarks of cancer?

A

1) sustaining proliferative signalling
2) evading growth suppressors
3) resisting cell death
4) enabling replicative immortality
5) inducing angiogenesis
6) activating invasion and metastasis

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6
Q

why is sustaining proliferative signalling useful? and how does it happen?

A

can become self sufficient at growth

  • endogenous growth factors
  • mutated growth factor receptors so always turned on
  • over express growth factors so respond to tiny amounts
  • mutate intracellular pathway so always activated
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7
Q

what is the therapy target for sustaining proliferative signalling?

A

EGFR inhibitors

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8
Q

how do they evade growth suppressors?

A

resist tumour suppressor genes -

  • Rb controls cell cycle progression
  • p53 halts cycle if not normal
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9
Q

what is the therapy target for evading growth supressors?

A

cyclin dependant kinase inhibitors

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10
Q

how do cells resist cell death?

A

-avoid caspase cascade

  • extrinsic pathway via death receptors
  • intrinsic pathway from DNA damage
  • resistance to anti-cancer drugs
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11
Q

what is the therapy target for resisting cell death?

A

Pro-apoptic BH3 mimetics

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12
Q

how do cells enable replicative immortality?

A

telomerase adds telomeres on

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13
Q

what is the therapy target for replicative immortality?

A

telomerase inhibitor

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14
Q

how does a tumour induce angiogenesis?

A

secretes vascular endothelial growth factor (VEGF)

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15
Q

what is the therapy target for angiogenesis?

A

VEGF inhibitor

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16
Q

what is the therapy target for invasion and mets?

A

HGF / c-met inhibitor

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17
Q

What are the 4 emerging hallmarks?

A

1) deregulating cellular energetics / reprogramming energy metabolism
2) evading immune destruction
3) genome instability and mutation
4) tumour promoting inflammation

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18
Q

What is the therapy target for deregulating cellular energetics?

A

aerobic glycolysis inhibitors

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19
Q

what is the therapy target for evading immune destruction?

A

immune activating anti-CTLA4 mAb

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20
Q

what is the therapy target for genome instability?

A

PARP inhibitors

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21
Q

what is the therapy target for tumour promoting inflammation?

A

anti-infl drugs

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22
Q

how may inflammation promote tumours?

A

provides growth factors, cytokines and immuno suppression

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23
Q

what are the characteristics of a feline injection site sarcoma?

A
  • previous FeLV or rabies vax
  • at site of inj
  • non painful
  • firm
  • fixed
  • locally invasive
  • cystic
  • fast growing
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24
Q

How do you diagnose a feline injection site sarcoma?

A

incisional biopsy

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25
Q

what is the 321 rule with feline injection site sarcomas?

A

its likely to be one if its over 3 months since a vax, over 2 cm and has increased in size 1 month post vax

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26
Q

why is cytology not useful at diagnosing feline infection site sarcomas?

A
  • as cystic so may just take cystic fluid so not representative
  • cant grade it
  • if under a month since vax then inflammation may still become neoplastic
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27
Q

why would you not do an excisional biopsy to diagnose feline injection site sarcoma?

A
  • no long term benefit
  • can affect prognosis as with second curative surgery may have mets, inflammation and fibrosis, seeding through tissue planes and will need larger margins, altered anatomy, less tissue to close with
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28
Q

how do you treat feline injection site sarcomas?

A
  • radical 1st surgery with 3-5 cm margins

- adjuvant radiation for 3-4 w

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29
Q

how can you avoid feline injection site sarcoma?

A

dont over vacc
dont repeatedly vaccinate in the same location
put vax in distal rear limb
use adjuvant free vax

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30
Q

what can cytology tell you / not tell you?

A

tell you - cell type, morphology

not - architecture, mitotic index, invasion, vasculature / lymph

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31
Q

What can histopathology tell you?

A 
cell type
morphology
tissue architecture
mitotic index
vasculature / lymph
necrosis
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32
Q

what are the 3 main categories ?

A

epithelial
mesenchymal
round cell

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33
Q

what is an epithelial tumour called?

A

carcinoma

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34
Q

what is a mesenchymal tumour called?

A

sarcoma

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35
Q

what information is used to grade a tumour?

A 
mitotic index
cellular differenatiation
invasion of surrounding tissues
vascular / lymph
necrosis
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36
Q

how is a tumour stages?

A

TNM

  • T = primary tumour size (T1-3)
  • N = regional LN (N0 = no mets , N1 = mets)
  • M = distant mets (M0=none , M1=some)
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37
Q

what is paraneoplastic syndrome?

A

systemic effects of a tumour, occuring at sites distant to the tumour due to hormones, cytokines or enzymes from the tumour

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38
Q

what can high calcium cause?

A 
PU/PD
anorexia
depression
weakness
bradycardia
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39
Q

What can low glucose cause?

A

weak
collapse
seizures

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40
Q

What can viscose bloody cause?

A

neuro signs

retinal detachement

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41
Q

What is neoplasia?

A

a monoclonal, uncontrolled proliferation of cells that continues in the absence of the inciting cause

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42
Q

what is seen grossly with a benign tumour?

A 
grow by expansion
slow growth
well demarcated
smooth outline
CT capsule
freely mobile
homogenous cut surface
little haemorrhage or necrosis
surgical removal easy
no recurrence if fully excised
no metastasis
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43
Q

what is seen grossly with a malignant tumour?

A 
grow by invasion
ulcerative on surface
not encapsulated
not mobile on palpation
necrosis and haemorrhage
removal difficult
often recurs
mets
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44
Q

what is seen micrscopically with benign tumours?

A 
similar to tissue of origin
well organised
can be functioning
doesnt breach capsule
few / no mitotic cells
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45
Q

what is seen microscopically with maliganant tumours?

A 
loss of cohesiveness and structure
no capsule
increased mitotic index
variable cell size +shape = pleomorphism
variable nuclei size +shape = anisokaryosis
increased nucleus : cytoplasm ratio
prominent nuclei
multinucleated syncytia
necrosis
fibrosis
inflammtion
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46
Q

what is a benign surface and gut ep tumour?

A

papilloma

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47
Q

benign glandular ep?

A

adenoma

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48
Q

malignant surface and gut ep

A

carcinoma

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49
Q

malignant glandular ep

A

adenocarcinoma

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50
Q

fibrous benign

A

fibroma

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51
Q

bone benign

A

osteoma

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52
Q

cartilage benign

A

chondroma

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53
Q

adipose benign

A

lipoma

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54
Q

smooth muscle bening

55
Q

endothelium benign

A

haemangioma

56
Q

skeletal muscle benign

A

rhabdomyoma

57
Q

fibrous malignant

A

fibrosarcoma

58
Q

bone malignant

A

osteosarcoma

59
Q

cartilage malignant

A

chondrosarcoma

60
Q

adipose malignant

A

liposarcoma

61
Q

smooth muscle malignant

A

leiomyosarcoma

62
Q

endothelium malignant

A

haemangiosarcoma

63
Q

skeletal muscle malignant

A

rhabdomyosarcoma

64
Q

what is a granuloma?

A

chronic inflammation

65
Q

what is a lymphoma?

A

malignant tumour of lymphoid system

66
Q

what is a melanoma

A

benign or malignant melanocyte tumour

67
Q

what is leukaemia?

A

tumour from bone marrow cells and circulates in blood

68
Q

what is a teratoma?

A

germ cell tumour with eco/endo/meso derm

69
Q

what is a sarcoid?

A

equine skin low grade fibrosarcoma

70
Q

how do carcinomas metastasise?

A

in the lymphatics

draining LN has some deposits

71
Q

how do sarcomas metastasise?

A

in blood

seeds to other organs

72
Q

how do mesotheliomas spread?

A

across serosal surfaces

73
Q

what does a high grade mean?

A

poorly differentiated

worse prognosis

74
Q

what does a low grade mean?

A

well differentiated

better prognosis

75
Q

what is chemotherapy?

A

cytotoxic drugs used in cancer treatment that interfere with cell growth / division of rapidly dividing cells

76
Q

what are the indications for chemotherapy?

A
  • primary treatment for disseminated disease
  • adjuvant therapy after surgery for highly metastatic tumours
  • after incomplete resection
  • neo-adjuvant to shrink before surgery
  • treatment of inoperable tumours
  • primary treatment for transmissible venereal tumour
77
Q

how does chemotherapy work?

A

affects different stages of the cell cycle

works best on actively dividing cells with a high mitotic index

78
Q

when is it best to use chemotherapy?

A

early on in disease when the cells are still dividing

79
Q

what is the cell kill hypothesis?

A

cell killing follows a first order kinetics so a given dose will kill a fixed percentage of the tumour population

80
Q

why do we pulse dose chemotherapy?

A

to allow times in between for normal tissue to recover but not enough time for tumour to regrow

81
Q

why do we use combination chemotherapy?

A

to avoid resistance

drugs to act on different parts of the cell cycle

82
Q

what are the 4 stages of chemotherapy?

A

1) induce
2) maintenance
3) re-introduction
4) resuce

83
Q

what are 2 alternative chemotherapies?

A
  • metronomic / continuous low dose chemo

- receptor tyrosine kinase inhibitors

84
Q

what is metronomic / continuous low dose chemo?

A
  • almost continual low dose given with a NSAID
  • aim is to slow growth by inhibiting angiogenesis
  • tumours may not shrink but disease should become stable
85
Q

what are 4 factors affecting chemo success?

A
  • tumour type
  • penetration of drug into tumour
  • development of drug resistance
  • multi drug resistance
86
Q

what are 4 common adverse effects of chemo?

A
  • myelosuppression
  • GI toxicity
  • poor hair growth
  • drug extravasation(outside vein)
87
Q

when will neutrophils and platelets be at their lowest after chemo?

A

neutrophils - 7d

platelets - 10 d

88
Q

what do you do if chemo has induced vomiting?

A

bland diet
gut protectant
anti-emetics

89
Q

what do you do if chemo has induced diarrhoea?

A

bland diet

metronidazole

90
Q

what do you do if the drug is know to affect the chemoreceptor trigger zone (CTZ)?

A

give phrophylactic anti-emetics

91
Q

How do alkylating agents work?

A
  • not cell cycle specific
  • replaces alykyl group with H+ in DNA causing cross linkage and DNA breakage
  • interferes with replicaiton / transcription
92
Q

what are some examples of alkylating agents?

A 
cyclophosphamide
lomustine
melphalan
chlorambucil
procarbazine
dacarbazine
93
Q

what is cyclophosphamides specific toxicity?

A

haemorrhagic cystitis in dogs

give plenty of water and chance to urinate

94
Q

what is lomustines toxicity?

A

hepatotoxicity in dogs (monitor ALT)

nephrotoxicity

95
Q

what do mitotic spindle inhibitors do?

A

cell cycle specific

binds to tubulin so prevents normal microtubule assembly

96
Q

what are some examples of mitotic spindle inhibitors?

A

vincristine
vinblastine
vinorelbine
taxanes

97
Q

what is vincristines toxicity?

A

peripheral neuropathies

cat constipation

98
Q

how do anti-metabolites work?

A

cell cycle specific

mimic normal substrates needed for nucleic acid metabolism so interfere with DNA synthesis

99
Q

what are some examples of anti-metabolites?

A 
cytosine
methotrexate
hydrocarbameide
5-fluoruracil
gemcitabine
azathiopine
100
Q

what is 5-FU toxicity?

A

cat nephrotoxicity

101
Q

what do anti-tumour antibiotics do?

A

prevent DNA and RNA synthesis

102
Q

what are some examples of anti tumour antibiotics?

A

doxorubicin
epirubicin
mitoxantrone
actinomycin

103
Q

what is doxorubicins toxicity?

A

cardiotoxicity in dogs
mast cell degranulation
nephrotoxic

104
Q

what do platinum compounds do?

A

cell cycle non specific

cause inter and intra strand crosslinks so affects synthesis and transcription

105
Q

what are some examples of platinum compounds?

A

cisplastin

carboplatin

106
Q

what is the toxicity of platinum compounds?

A

pulmonary oedema
nephrotoxic
vomiting

107
Q

what would you give corticosteroids to help neoplasia?

A

apoptosis of lymphoid and mast cells

108
Q

what would you give L-asparginase to neoplasia?

A

neoplastic lymphoid cells rely on L-aspargine

109
Q

what would you give NSAIDs to neoplasia?

A

inhibit angiogenesis
promote apoptosis
anti infl
analgesia

110
Q

why would you give receptor tyrosine kinase inhibitors?

A

interfere with cell signalling needed for cell growth, proliferation and survival

MCT esp

111
Q

when is a biopsy indicated?

A

if treatment would be affected by tumour type

owners willingness affected by prognosis

112
Q

guidelines for biopsy

A
  • dont compromise further treatment
  • dont breach fresh anatomic planes
  • use fresh instruments for each site
  • include normal and abnormal tissue
  • try not to deform specimen by forcceps
  • tissue should be <1cm thick in 10%formalin
113
Q

what is prophylactic surgery?

A

removal of a tissue which will reduce tumour incidence

e.g gonadectomy or suspected pre-cancerous lesion

114
Q

what are the advantages and disadvantages of curative surgery?

A

+ = immediate cure, not carinogenic, no local toxicity, not immunosupressive, remove large mass

  • = local cure only, change in cosmeis, change in function
115
Q

what are the principles of curative surgery?

A
  • plan surgery and reconstruction
  • do as early as possible
  • first surgery has best chance
  • good margins in all 3 dimension
  • dont compromise margins for cosmesis
116
Q

8 practical considerations for curative surgery

A

1) cosmesis and function
2) pre-op preparation (dont scrub too hard as disseminate, Abx?)
3) dissection technique (atraumatic)
4) reduction of contamination (dont handle tumour, change to clean gloves etc for closure)
5) avoid wound complications (be gentle)
6) vascular occlusion (prevent diseemination)
7) LN removal for staging
8) reconstruct defecit

117
Q

what is a local excision? and indications?

A

tumour removed through its natural capsule with minimum adjacent tissue

benign tumour with no tendency to infiltrate

118
Q

what is a wide local excision? and indications?

A

tumour removed with appropriate margins, dont enter clean fascial planes

benign infiltrating, malignant non infiltrating

119
Q

what is radical local excision and indications?

A

tumour removed on all aspects with a clean fascial plane - compartmental, muscle group, amputation

tumours with a pseudocapsule

120
Q

what is cytoreductive surgery?

A 
planned incomplete removal to improve efficacy of other treatment 
or
retain essential anatomy
or
tumour highly likely to recur
121
Q

what is pallative surgery?

A

improve quality but not always length of life

pain relief

122
Q

what are the indications for radiation?

A

incompleteley resected tumour
shink non resectable tumours
pain control (destroys recceptors)

123
Q

how does radiation work?

A

induces direct and indirect DNA damage

want damage bad enough to cause cell death, or alive but cant divide

124
Q

Why do we fractionate radiations? (4Rs)

A

spares normal tissue because it allows repair of sublethal damage and repopulation

increases damage to the tumour because of reoxygenation and redistribution of cells into radiosensitive phases of cells cycle

125
Q

what is reoxygenation in regards to radiation?

A

only the vascularised cells on the tumour periphery are affected by radiation so the necrotic core has more room so outside becomes perfused so can then destroy that.
therefore we fractionate

126
Q

what is a curative dose of radiation?

A

2-3 Gy / d for 3 w

127
Q

8 neoplasms that can be cured with radiation? (maybe with surgery combined)

A 
nasal tumours
brain tumours
oral tumours
sq cell tumours
epulis
soft tissue sarcoma
feline injection site sarcoma
oral fibrosarcoma
128
Q

what is an epulis?

A

benign tumours of gingiva / alveolar

129
Q

what is a pallative radiation dose?

A

6-7 Gy/week for 4w

130
Q

3 reasons that radiation can be used pallatively for

A

radiosensitive tumours with high mets rate
shrinking mass effect
pain control (esp in bone)

131
Q

what are the acute side effects of radiation?

A
  • skin - erythema, dermatitis, alopecia (collar and analgesia)
  • MM - hypersalivation, discharge, mucositis (analgesia, feeding tube)
  • eyes - conjuctivitis, blepharitis, cornea ulceration (optimmune treatment)
  • CNS - edema, transient demyelination (corticosteroids)
132
Q

what do acute radiation effects appear and go?

A

see them 7-10 d post treatment

self limiting and resolve in a few weeks

133
Q

what are the late side effects of radiation?

A
  • Skin - fibrosis, alopecia, pigment changes
  • eyes - cataracts, chronic keratoconjunctivitis sicca
  • CNS - necrosis of white matter, vasculopathy
134
Q

What are the late side effects of radiation seen?

A

after 6 months

year 3 principles (20 decks)

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