198: Phototherapy Flashcards
What are the main types of phototherapeutic devices used in phototherapy?
The main phototherapeutic devices include Broadband UVB (BB-UVB), Narrowband UVB (NB-UVB), Ultraviolet A (UVA), and Psoralen photochemotherapy (PUVA).
How does UVB radiation affect the skin and immune system?
UVB radiation (290 to 320 nm) is absorbed by the epidermis and superficial dermis, produces DNA damage, mediates UVB-induced immunosuppression, increases hydroxyvitamin D synthesis, and affects signal transduction pathways.
What is the significance of reactive oxygen species (ROS) in UVA radiation exposure?
UVA radiation (320 to 400 nm) generates ROS, which exceed neutralization by protective activities, are implicated in photoaging and skin cancer, and have immunoprotective properties in animal studies.
What are the effects of psoralen photochemotherapy on DNA?
Psoralen photochemotherapy intercalates with DNA upon UVA activation, forming adducts that crosslink DNA strands, inducing DNA damage and reactive oxygen intermediates.
How does phototherapy influence the immune system?
Phototherapy generates effector and regulatory T cells, with the immune response intensity dependent on their proportions, and can lead to immunosuppression.
What are the main phototherapeutic devices used in phototherapy and their respective wavelengths?
The main phototherapeutic devices and their wavelengths are: Broadband UVB (290 to 320 nm), Narrowband UVB (310 to 315 nm), UVA (320 to 400 nm), and PUVA (UVA range with psoralen activation).
How does UVB radiation affect the skin and what types of DNA damage does it produce?
UVB radiation affects the skin by being absorbed superficially and producing DNA damage, including pyrimidine dimers and 6,4-pyrimidine-pyrimidone photoproducts.
What is the significance of reactive oxygen species (ROS) generated during UVA radiation exposure?
ROS generated during UVA exposure are significant as they contribute to photoaging and skin cancer and exceed the neutralization capacity of protective activities.
What role does psoralen play in photochemotherapy and how does it interact with DNA?
Psoralen intercalates with DNA when activated by UVA, forming adducts that crosslink DNA strands, leading to DNA damage.
How does UVB radiation influence vitamin D production in the skin?
UVB radiation increases hydroxyvitamin D synthesis, inversely correlating with trans-urocanic acid levels.
What are the immune system effects of phototherapy under normal circumstances?
Phototherapy generates both effector and regulatory T cells, with the immune response intensity dependent on their relative proportions.
What are the clinical implications of the different depths of penetration of UVB and UVA radiation?
UVB primarily affects the epidermis and superficial dermis, while UVA penetrates deeper, reaching the mid-dermis.
What are the potential side effects of phototherapy related to UV radiation exposure?
Potential side effects include short-term sunburn-like reactions, long-term skin cancer risks, and possible immunosuppression.
How does the generation of reactive oxygen intermediates during phototherapy relate to skin damage?
Reactive oxygen intermediates cause oxidative stress, leading to DNA damage and contributing to photoaging and skin cancer.
What is the relationship between UVA radiation and the production of heme oxygenase-1 in animal studies?
UVA radiation induces heme oxygenase-1 production, which has immunoprotective, antioxidant, and anti-inflammatory effects.
What is the effect of UVB exposure on effector and regulatory T cells?
UVB exposure inhibits effector T cell activation while leaving regulatory T cells unaltered, diminishing cell-mediated immune response.
How does UVA1 affect mast cells compared to PUVA?
UVA1 causes apoptosis of mast cells, reducing their concentrations, while PUVA stabilizes mast cell membranes.
What are the effects of phototherapy on collagen production?
Phototherapy activates MMP-1 and increases IL-1 and IL-6 production, enhancing collagen remodeling.
What changes occur in keratinocytes due to UVB, PUVA, and UVA exposure?
These exposures cause acanthosis of the epidermis and thickening of the stratum corneum.
What role does interleukin-10 (IL-10) play in the immune response following UV exposure?
Increased IL-10 levels serve as an immunosuppressive factor, diminishing dendritic cell antigen presentation.
What is the effect of UVB exposure on the activation of effector T cells and regulatory T cells?
UVB exposure inhibits effector T cell activation while leaving regulatory T cells unaltered.
How does UVB exposure affect dendritic cells and their role in T cell responses?
UVB exposure disrupts dendritic cell activities, diminishing their capacity to present antigens.
What are the immunosuppressive soluble mediators that increase following UVB exposure?
Following UVB exposure, mediators such as platelet activating factor receptor agonists, MSH, CGRP, and IL-10 increase.
What is the role of Prostaglandin E2 in the context of UVB exposure?
Prostaglandin E2 acts as an inductive stimulus for cyclooxygenase-2, which is lowered by UV exposure.