RT-theory Flashcards
What kind of radiation beams can be produced by a Linear accelerator?
High energy x-ray and electron beams
What kind of radiation is brachytherapy?
It uses I131 and produce beta-particles (electrons and positrons)
High-energy beams (photons) deposit energy ______
at a greater depht than eletrons
Low-energy beams (electrons) deposit most of the energy_______.
Skin surface
Name the 3 processes by which x-ray photons give up their energy when interacting with tissue?
Photoelectric effect, compton effect, paired reduction
What is the definition of Gy?
1 Gy = 1 J/kg (1 joule absorbed per kg)
Define LET?
Linear energy transfer = average energy lost by a particle over a given track length
The biologial effect of a dose of radiation depends on its LET
Give an example of a low LET particle and a high LET particle?
low = photons
high = protons
How can DNA be damaged by radiation?
Direct - absorption of energy by DNA
Indirect- damage via free radicals
Which radical is most damaging for DNA
Hydroxyl radixal - oxidising
How many doble strand breaks are achieved pr. 1Gy?
only 25-50
What is mitotic cathastrophy?
Occur due to chromosomal aberrations secondary to DNA DSB
What is the bystander effect?
When ROS or other factors are released from irradiated cells, causing damage to nearby non-irridated cells
By which two mechanisms can DNA DSBs occur and what are they called?
Passage of sinfle paricle = linear effect - seen most with low dosages
Passage of two separat particles causing a SSB = quadratic component - high dose
What is the alpha-beta ratio?
Its where the killing via the one hit(linear) and two hit (quadratic) kinetics are equal
Which tumours are considered to have a low a/b ratio?
melanoma, prostatic tumour, STS, TCC, OSA
By which modes can a cell die after RT and which one is most common?
Apoptosis, necrosis, miotic cathastrophe (most common), terminal growth arres
Which 4 cell types are particularly sensitive to apoptotic death?
Lymphocytes
Thymocytes
Salivary gland epithelium
Spermatozoa
Where in the cell cycle are the cells most senistive to radiaion?
M-phase (and late G2)
Why are cells in S-phase more resistant to radiation?
Due to increasd DNA repair in this phase
Which drugs can increase radiosensitisation?
Imatinib
PARPi
Carboplatin
Gemcitabine
Defnine the following:
CRT
3D-CRT
IMRT
SBRT
Brachy
Plesio
CRT- uniform intensity across the RT beam, square
3D-CRT - uniform intensity, irregular beam shape
IMRT - variying intensity of the beam, irregular shape
IGRT - IMRT which changes the size shape and location of tumour or other organs
SBRT - highly conformal, often RT administered in 1-5 fractions
Brachy - directly adjacent tumour or within
Plesio - source of RT placed in contact with exterior surface of the body
GTV
Gross tumour volume
CTV
Clinical target volume - allows for tx of microscopic disease beyond edge of visible tumour, or metastatic disease
PTV
Planned target volume - GTV + CTV + additional margin for set up error, patient movement etc
By which cellular mechanisms are DSBs repaired?
Homologous recombination - S and G2
Non-homologous end joining - throughout cell cycle
What are the risks of SRT?
Higher risk of late effects due to high dose in few fractions - it is fractionation and allowing repair which spares the normal tissues
What are the reasons combining RT with other treatments may improve outcome?
- Prevent repopulation
- Decrease clonogenic tumour cells
- Increase cellular rt sensitivity
- Improve reoxygenation
- Kill circulating endothelial precursor cells which would replace vasculature destroyd during RT.
Name 5 factors impacting tumour senistivity to RT
- Number of CSC - increased nr = increased RT dose needed
- Degree tumour hypoxia
- Genetic/epigenetic heterogeneity
- Degree of expression/acivation of intracellular pathways (EGFR/MEK/ERK adn PI3K/AKT)
- Vascular damage - pro (deprivation of nutrients and cell death con increased hypoxia
What is the beneficial effect of hypoxia?
The biological effect of RT are enhanced by oxygen
Oxygen can fix the DNA damage caused by hydroxyl radicals and lead to irreparable damage.
What are the drugs nimorazole and tirapazamine?
Hypoxic cell senzitiser
Drug toxic ony to hypoxic cells
When is the cut of between early, early delayed and delayed responses for RT?
Acute - less than 3 in rapidly dividing cells
Early delayed - 2 w and 4 months (only neurological tissue)
Late response - over 3 months in slowly dividing cells
What are consequential late effects?
When severe early reactions result in impaired tissue recovery
Which factor influence the risk of acute tox the most?
By the time over which a protocol is administered (and total dose)
Which factors impact the risk of late tissue tox the most?
Fraction size, volume of tissue irradiated and total dose
What are functional subunits?
How one consider some late responding tissues - arranged in parallel (lung, liver, kidney) or series (spinal cord, intestine)
Is it parallel or series tissue which have a reserve capasity when it comes to late RT effect?
Parallel
What is amifostine?
Drug that can be used to reduce sensitivity of normal cells to RT, without influencing tumour cll sensitivity
What are the 5 Rs of radiation
Repair
Repopulation
Reoxygenation
Redistribution
Radiosensitivity
Hyperfractionated
o Involves giving a larger total dose
o Fraction size reduced; number of fractions increased
o Treatment time is the same
o Allows higher tumour control (due to higher total dose), whilst reducing late toxicity
What is BED used for?
A calculation used to predict how changes in dose prescription may affect different cells/tissues based on their alpha/beta ratio
