Radiation Injury Flashcards
Late toxicity is permanent, occurring 6 months after the
completion oftherapy
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Brachytherapy,
utilizing radium,
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the cobalt-60
unit skin-sparing capability, and improved homogeneity of dosage
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dose-response relationship between tumor
control and normal tissue complication is known as the therapeutic
ratio
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it is accepted that normal tissue will have a 5% risk ofcomplication
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As described earlier, RT affects cells through molecular injury either
by direct disruption of the DNA structure or through ionization
of an intermediary, producing free radicals to interact and damage
DNA.
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DNA damage preferentially affects cells during the proliferative.
phase of the cell cycle, therefore primarily affecting cells with rapid
turnover such as oral mucosa and epithelium.
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The pathophysiology of the acute toxicity is
from free radicals and irreversible breaks in DNA
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In the skin, injury can also affect the epidermal permeability barrier, facilitating increased entrance of toxins and antigens
to aggravate dermal inflammation, and can predispose the epider�s
to infections
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Skin injury occures imediatly after radioation
injury presents 2 to 4 weeks after the m1-
tiation of therapy
Acute radiation injury is dependent on the dose of radiation, volume of
tissue irradiated, or concurrent chemotherapeutic drug use
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healing beginning at about 2 weeks
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With high dose of radaition there wil be damag to the progenators stem cells that lead to irreversible damage termed consequential
damage and can present as ulceration or necrosis to the site of radiation toxicity.
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there can be a delayed acute toxicity in
certain tissues. Examples include acute radiation pneumonitis, which
occurs 8 to 16 weeks following the initiation of radiation temporary demyelination ofthe posterior columns during
spinal irradiation, presenting 2 to 6 months following RT
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temporary demyelination ofthe posterior columns during
spinal irradiation, presenting 2 to 6 months following RT
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