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Radiobiology Flashcards

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1
Q

what are the three phases within the body

A

physical, chemical, biological

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2
Q

describe the physical phase

A
  • CS
  • x-rays/ gamma rays remove an atom due to an interaction with an orbital electron, this vacancy is then filled by an inner electron via CR. The scattered photon continues interacting as well as releasing an electron
    10^-18 cross DNA
    10^-14 sec to cross cell
  • leads to chemical change
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3
Q

describe chemical change

A
  • H2O causes indirect DNA damage
  • change within the body
  • occurs before the patient leaves the room
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4
Q

describe the biological phase

A
  • won’t see a change for a few days
  • direct damage, partial interactions, within DNA + indirect damage (cell kill)
  • cell cycle damage
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5
Q

what happens with SSB

A

the backbone is broken affecting only one strand

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6
Q

what happens with DSB

A

there is a break at either side, damaging the nitrogenous base, which affects both stands
- only a small proportion of damage

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7
Q

why is DSB vital

A

in order for cell kill

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8
Q

what does 1-2 Gy result in

A

1000 SSB = 40 DSB

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9
Q

describe direct DNA damage

A
  • x-rays only slightly damage the DNA
  • higher doses are needed
  • direct ionisation occurs at the critical target of DNA
  • DNA damage, breaks the crosslinks between DNA and protein
  • chromosome aberrations - breaking and rejoining of chromosomes, sticky ends join with sticky ends creating a distortion
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10
Q

describe indirect damage

A
  • chemical change
  • X-rays / photons by products of water
  • secondary electrons ad protons (interact with tissue)
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11
Q

name highly sensitive tissue

A
  • epithelial lining of the alimentary canal
  • haemapoetic tissue
  • reproductive cells

these demonstrate damage in 3-4 days
epithelial skin damage is within 7-10 days

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12
Q

where are SSB repairable

A

checkpoints

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13
Q

what is the irradiated volume

A

it is the normal tissue which receives a significant dose

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14
Q

what is the therapeutic ratio

A

ratio between normal and tumour cell damage. Effects of tumour response and normal tissue damage

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15
Q

what happens to the tumour response as dose increases

A

it increases

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16
Q

how does tissues differ within the SI

A

both tumour and normal cells are responsive within the SI which causes more damage causing a greater effect

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17
Q

do tumours and normal cells differ in affected by radiation

A

they act in the same way but tumour cells become damaged at a lower dose

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18
Q

what happens with radio-sensitivity and radioresistant

A

if the tumour is radio resistant (T shifts right) or if normal cells are radiosensitive (C shifts right), lowering the tumour response.

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19
Q

why are radio-resistant tumours less likely to be treated with RT

A

more normal tissue would be irradiated as higher doses are needed

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20
Q

considerations

A
  • early effects = skin erythema
  • late effects = telangectasia
  • initial x-ray deposition occurs rapidly
  • eye lens is radiosensitive
  • the latent period after irradiation is inversely related to the dose administered and ranges from minutes to years
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21
Q

what is radio-sensitivity

A
  • relative vulnerability of cells which are damaged by IR
  • number of cells killed by the dose
  • dependent on cell type (malignant or normal), histology
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22
Q

which structures have intermediate sensitivity

A
  • lung
    -kidney
  • eye lens
  • supportive nervous tissue
  • demonstrated within a week or so
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23
Q

low sensitivity structures

A
  • muscle
    -bone
  • connective tissue
  • nervous tissue
  • slow reproduction rate
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24
Q

what is the standard regime involve fraction wise

A

2 Gy

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25
Q

what are the four R’s

A

Reoxygenation
Reassortment
Recovery
Repopulation

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26
Q

Describe re-oxygenation

A
  • applies to the tumour cells
  • hypoxic cells gain access to oxygen which causes DNA fixation damage
  • low O2 = tumour reaper, indirect damage causing SSB
  • increased susceptibility to radiation damage
  • occurs within 24 hours
  • daily treatment gives a better response
  • links with angiogenesis
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27
Q

describe re-assortment

A
  • occurs over a few hours
  • M phase is twice as sensitive as the late S cells
  • single fractions kills cells preferentially
  • RT is cell specific
  • increases chances of hitting cell in a sensitive stage
  • single exposure damages fewer cells
  • radiation introduces a block in G2
  • checkpoint ensure successful replication otherwise cell apoptosis
28
Q

describe recovery

A
  • all cells repair radiation damage
  • can recover from SSB
  • occurs over a few hours
  • normal cells have a higher capacity at recovering after a fractionation
29
Q

describe repopulation

A
  • allows for proliferation of tumour cels
  • shorter RT has less repopulation, resulting in higher doses in order for cell kill
  • everyday of fractionated RT over 3-4 weeks results in a loss of 0.6 Gy so an additional 0.6 Gy must be given at each fraction
30
Q

what are the factors of biological radiation doses

A

number of fractions
total dose
TT

31
Q

what are tissue tolerances

A

the degree of risk which is independent on the seriousness of the resultant disease
- < or equal to 2cm included in the tangential fields
- 5% risk of bowel damage is acceptable for CA cervix
- < or equal !% spinal cord damage is acceptable
- cataract formation occurs 100% patients who receive 7 Gy to the lens

32
Q

what are low tolerances equal to

A

radiosensitive tissue

33
Q

when are low doses given

A

whole organ irradiation

34
Q

when are high doses given

A

partial organ irradiation

35
Q

what are oxic cells

A

fully oxygenated cells

36
Q

what are anoxic cells

A

cells which lack oxygen

37
Q

what are hypoxic cells

A

poorly oxygenated cells

38
Q

what happens beyond the anoxic region

A

necrosis, so some tissue will die

39
Q

what is acute hypoxia

A

hypoxia which is temporary when capillaries open and close, this occurs randomly

40
Q

describe chronic hypoxia

A
  • angiogenesis is not well developed
  • cells may proliferate well, dead
  • responses vary
  • cells won’t reoxygenate
41
Q

what determines the amount of radiation given

A

normal tissue tolerance

42
Q

what is classed as category 1

A
  • radical intent, with prolongation likely to adversely affect the outcome
  • NO unscheduled interruptions
  • SCC H&N, SCC cervix, medulloblastoma
43
Q

what is classed as category 2

A
  • radical intent, no clear evidence that prolongation will adversely affect the outcome
  • should be kept to a minimum
  • IF there’s a break it needs to absolutely necessary
44
Q

what is classed as category 3

A
  • palliative intent
  • no evidence that it will cause affect
  • hypo fractionated
  • less impactful
45
Q

what is the tolerance dose

A

max amount of radiation a tissue can receive before becoming permanently damaged

46
Q

what is tolerance dose dependent on

A
  • radiation type
  • tissue type
  • fractionated
47
Q

what is angiogenesis

A
  • formation of new blood vessels
    any tumours over 400um
48
Q

background info on oxygen effect

A
  • broad beans were irradiated in a surplus supply of oxygen as well as a deficit
49
Q

why is being in an oxygenated environment beneficial

A
  • allows for more DSB
  • capillaries supply oxygen to toxic tissue
  • cells irradiated in an absence of oxygen tend to be more radioresistent, so more susceptible to damage
  • tumours are capable of VEGF, (vascular epithelial growth factor), enoucrgaing capillary growth
50
Q

give the radiolysis process

A

O2 + OH. -> free radical preventing sublethal damage
R. + O2 -> RO2.

(RO2. causes permanent DNA damage)

51
Q

what is oxygen classed as?

A

a fixer, it fixed damage in place making it permanent
hypoxic cells are less reactive

52
Q

what is the gold standard for breast cancer

A

40 gray, 15 fractions

53
Q

what mmHg is most beneficial

A

20

54
Q

what is the oxygen enhancement ratio

A

how sensitive cells are when fully oxygenated
typical = 2.5-3

55
Q

equation for OER

A

OER = hypoxia/ oxia

56
Q

what is the max ppO2 in well vascularised tissue

A

40 mmHg

57
Q

what is the bystander effect

A

cell survival is reduced when communicating with adjacent irradiated cells. Bystander 1: cells receiving a low dose during RT exhibit increased survival when neighbouring cells receive a lethal dose

58
Q

conventional RT

A
  • 2 gy per fraction
  • 20-25 fractions
  • 35-40 fractions
59
Q

hyPOfractionated

A
  • under fractionated, high doses
  • less frequent RT
  • single exposure = 8 Gy per fraction, once weekly, twice for NSCLC
  • bone metastases = 15 gy single exposure
  • 3.3-3.6 Gy per daily fraction, total 15 fractions
  • radioresistent tumours
  • not used in head and neck
60
Q

HyPERfractionated

A
  • more than one fraction per day
  • 6 hour gap due to serious tissue damage/ late morbidity, allows reoxygenation
  • no more than 3 a day
  • head and neck
61
Q

CHART Wel

A
  • CHART weekend less
  • 1.5 Gu, 40 fractions
  • 3 fractions per day over 17-19 days, total of 60 Gy
  • head and neck and NSCLC
62
Q

continuous

A
  • no weekend breaks
  • hyperfractionated or conventional
  • reoxygenation can occur
  • addresses repopulation
  • management issues, lack of staff
63
Q

CHART

A
  • for short doubling time tumours
  • hyPERfractionated
  • 1.5 Gy/ 36 fractions
  • 3 fractions per day over 12 days = 54 Gy
64
Q

Accelerated

A
  • 5+ fractions per week
  • addresses recovery from sub-lethal damage in low LET
  • addresses repopulation: can’t repopulate
  • fractionation over 4 weeks must have higher doses
  • normal tissues can’t repair, increasing side effects
  • recurrence of tumour is hard to treat
65
Q

how is unscheduled gaps compensated

A
  • twice daily fractions min 6 hour gap
  • weekend treatment
  • BED, fewer fractions to achieve planned overall, dose is higher
  • additional fractions to compensate within the original TT, treatments are added
  • category 1 patients must be treated first twice daily

Physics (25 decks)

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