CANCER INTRODUCTION Flashcards

1
Q

which gender has most cancer overall

A

male

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2
Q

what is cancer

A
uncontrolled cell proliferation 
loss of natural apoptotic control 
decreased differntiation 
invasion 
ability to establish atypical environments 
loss of tissue organisation
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3
Q

How does cancer occur (3)

A

genomic instability
mutations
epigenetics

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4
Q

genes which can cause cancer

A

overexpression of oncogenes RAS or MYC,

faulty TSGs e.g. BRCA, p53

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5
Q

whats endogenous mutagenesis

A

chemical instability of DNA/ errors in replication

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6
Q

what can cause endogenous mutagenesis

A

oxygen free radicals produced in metabolism

lifetime exposure to oestrogen

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7
Q

other thing which can cause cancer- think more external

A

chemical carcinogens e.g. tabacco, environmental pollutants, alcohol
physical agenst such as UV or X-Rays
viruses and bactera e.g. HPV, H.pylori

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8
Q

what is epigenetics

A

means of altering the activity of genes by changing how compact or relaxed DNA is

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9
Q

effect of methylation

A

compacts DNA= reduced gene expression

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10
Q

effect of acetylation

A

relaxes- increases expression

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11
Q

ways proteins can cause cancer?

A

mutations

too much, too little, wrong place, less stable, more stable

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12
Q

what makes certain cells more prone to cancer?

A

as mutations occur in the S phase its more likley to occur in rapidly dividing cells e.g. epithelial lining of the gut
cells such as glial cells typically inhabit the g0 phase but can be stimulated to enter into division

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13
Q

what type of cells never divide?

A

myocardial

so unlikely to be cancer

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14
Q

4 classifications of cancer

A

Histopathology
grade
stage
metastasis

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15
Q

how to determine histopathology?

A

microscopic examination by biopsy

establishes origin of the disease and what type of cancer it is.

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16
Q

explain the grade of cancer? what makes it low or high grade? speed of growth?

A

low: well differentiated- look like normal cells, slow growth
high: less like normal cells, aggressive fast growth

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17
Q

what is staging? how do we present this?

A
how much of the disease is present 
TNM
tumour size
nodal envolvement 
metastases
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18
Q

TNM meaning and values

A

Tumour size 1-4, the bigger the side the higher the number
Nodal involvement 0 if local and 1 if <4 nodes and 2 if >4 nodes
Metastases either 0 or 1 if its gone into a different organ space- must be same cells as in primary tumour

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19
Q

3 ways of metastasis?

A

direct invasion- direct penentration through tissue
lymphatic spread
blood stream

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20
Q

generic presentation of cancer

A

lump
unexplained bleeding
weight loss

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21
Q

specific signs of cancer

A

chest pain

change in bowel habit

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22
Q

4 things that are used to confirm diagnosis

A

X-ray
biopsy
biomarkers
CT/PET

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23
Q

2 types of cancer surgery

A

palliative- to improve QOL

curative

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24
Q

what is curative surgery? would this be the only treatment?

A

primary tumour removal- no as high risk of relapse, probably chemotherapy

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25
Q

how would the tumours margins be classed as 0

A

in surgery the surgeon will take a sample from around the tumour, if no tissues found here the margins are 0

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26
Q

how do you qualify for palliative surgery? examples?

A

reasonable prognosis 3-6 months

e/g/ bowel obstruction

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27
Q

what can be used in place of surgery if the patient isnt fit enough?

A

radical radiotherapy- curative

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28
Q

what ways can radiotheapy be given in relation to surgery?

A

reduce size prioir to surgery

adjuvant: to consolivate surgery with chemo
palliative: to relieve symptoms of incurable disease

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29
Q

which type of radiotherapy is most common?

A

external beam radiotherapy

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30
Q

examples of external beam radiotherapy

A

Xray, electron, proton

31
Q

what is stereotactic radiosurgery

A

cyber knife, avoids effects on surrounding tissue

32
Q

what is total body irridiation?

A

fully ablate bone marrow before stem cell transplants

33
Q

advantages of proton beam radiotherapy

A

reduces amount of RT administered to surrounding tissues, able to calculate it specifically to hit the tumour
useful for tissues which dont regenerate well

34
Q

examples of internal radiotherapy

A

liquid radioiodine
selective internal radiation therapy (beads)
solid sources of RT
INTRACAVITY
interstitial- into tumour, stays forever and delivers radiation for 6-12 months

35
Q

would an interstitial seed of RT make the person radioactive?

A

no, works locally

36
Q

endogenous radiosensitiser?

A

oxygen: binds to breaks in DNA rendering them unfixable= cell death

37
Q

exogenous radiosensitiser?

A

chemoradiotherapy e.g. cisplatin
gemcitabine
temozolomide, capecitabine, cetuximab

38
Q

acute side effects of chemo?

A

rapidly dividing cells targetted: alopecia, N&V, indigestion, mucositis, taste disturbance, oesophagitis, diarrhoea, cystisis

39
Q

late effects of chemo?

A

slowly dividing cells

fibrosis, breathlessness, lymphodema, bladder/ bowel incontinence, vaginal stemosis, sterility

40
Q

when do acute side effects of RT present/ go away?

A

1-2 weeks into RT lasts for 3-4 weeks after

41
Q

skin reactions in RT can be made worse by which risk factors?

A

older, smoking, alcohol, malnutrition, obesity

42
Q

how to treat skin reactions? grades 1-4

A

grade1: moisturiser
2: m+ HYDROCORTISONE OR INSTILLAGEL
3: M, increase HC potency, dressings
4: consult

43
Q

managing oral hygiene on radiotherapy?

pain pf mouth?

A
mucositis
socium chloride/ bicarbonate, diflam
stop smoking 
brush BD
pain: mist paracetamol
44
Q

how to manage RT associated N&V

A

5-HT3 receptor antagonist from 24 hours prior and 24 hours after treatment
ondansetrn or metoclopramide/ domperidone

45
Q

low risk cancers for RT induced N&V? if prophylaxis used?

A

breast, head and neck, limb, brain, no prophylaxis used

46
Q

treating cystitis from RT

A

antibiotics

47
Q

treating diarrhoea from ABs

A

loperamide

48
Q

what is SACT

A

systemic anti cancer chemotherapy

49
Q

exampls of SACT

A

targetted agents
cytotoxic traditional chemo
immunotherapy
CAR-Ts

50
Q

what do cytotoxic agents affect

A

all cells- depends on cell cycle stage in some

51
Q

what must you do before giving targeted chemo?

A

establish expression of target, ensure to monitor for resistance

52
Q

how does cytotoxic ?

A

interfered with cell cycle

kills cells and healthy cells

53
Q

side effects of cytotoxic chemo

A

bone marrow suppression, N&V, alopecia, peripheral neyropathy

54
Q

example of cytotoxic chemotherapy

A

capecitabine, flurouracil prodrug

55
Q

capecitabine flurouracil MOA

A

antimetabolite, interfered with DNA replication enzymes

prevents thymidine production and halts DNA replication

56
Q

which types of cytotoxic chemo is associated with peripheral neuropathy

A

platinums and taxanes

57
Q

is alopecia and N&V seen with all cytotoxic drugs?

A

no, not all

N&V depends on emetogenicity of t he drug

58
Q

how do targetted agents work

examples

A

disrupt ssignalling pathways which allows cancer cells to proliferate
TKIs
mAbs

59
Q

what is gefitinib, what does it treat?

toxicities?

A

EGFR inhibitor, lung cancer, skin can give acneiform rash due to EGFR expression in the skin
GI disturbance

60
Q

Cetuximab MOA

treats?

A

EGFR inhibitor
needs RAS wild type
treats RAS wild type colorectal cancer, cant use if mutated RAS

61
Q

side effects of Cetiximab

A

acneform rash like TKI but no GI disturbances

hypersensitivity

62
Q

what is a targeted cytotoxic agent?

A

combines two MOAs to increase efficacy and reduce toxicity

binds due to target and then releases cytotoxic agent

63
Q

example of a targeted cytotoxic agent

A

trastuzumab HER2 receptor

64
Q

trastuzumab MOA

A

HER-2 receptor specific
delivers a cytotoxic moiety as well
binds to HER2 cells only then releases= specific

65
Q

what does immunotherapy utilise

A

T cells/ the immune cells

66
Q

T cells normal role, how does cancer stop them?

A

they seek and destroy

cancer can express PD-1 which normally prevents autoimmune activity, but cancer uses it so T- cells cannot destroy them

67
Q

how can we use immunotherapy to stop cancer deactivative T-cells using the PD-1 ligand?

A

PD-1 checkpoint inhibitor

68
Q

toxicities of PD-1 checkpoint inhibitor?

A

autoimmune like conditions
colitis
pneumonitis
hepatitis

69
Q

what is ATMP

A

advanced therapy medicinal products

70
Q

example of ATMPs (advanced therapy medicinal products )

A

A gene therapy medicinal product
A somatic cell therapy medicinal product
A tissue engineered product

71
Q

example of a ATMP

A

CAR-T

72
Q

what does CAR-T treat? how are they made?

A
leukaemia 
T-cells taken from patient 
engineered to recognise cancer cells 
cultured to increase number 
returned into patient to destroy cancer
73
Q

risk of using CAR-T cells

A

risk cytokine storm which can be life threatening

74
Q

example of surgery RT and CT being used? give drug names

A

breast cancer
surgery to remove primary tumour if caught early
adjuvant chemo for micro metastases
radiotherapy for unclear margins at chest calls
1 year of trastuzumab or herceptin if HER+]5 YEARS OF ENDOCRINE THERAPY IF HORMONE RECEPTOR +VE E.G. TAMOXIFEN