Final answer:
Peripheral sensitization in chronic pruritus results in an increased sensitivity of nerve fibers to itching stimuli, often due to inflammatory reactions from type I or delayed hypersensitivities to allergens or irritants. It is a key phenomenon in understanding and managing allergic reactions and contact dermatitis. Treatments may include desensitization therapy or medications to reduce inflammation and alleviate symptoms.
Step-by-step explanation:
Peripheral sensitization in chronic pruritus is a physiological process that amplifies the sensation of itch in response to stimuli. It involves the lowering of the threshold for activation of peripheral sensory nerve fibers that carry itch signals to the brain. This process is often triggered by inflammatory mediators released during an immune response to allergens or irritants.
In the case of type I hypersensitivities, such as allergic reactions to pollen or pet dander, exposure to the allergen causes the immune system to produce IgE antibodies. When re-exposure to the allergen occurs, these antibodies stimulate mast cells to release histamine and other mediators that can cause a wheal-and-flare reaction on the skin, which indicates pruritus sensitization.
For delayed hypersensitivities, typically associated with cell-mediated immune responses as seen in contact dermatitis or the tuberculin reaction, sensitized T-cells release cytokines that lead to an inflammatory response that can occur days after exposure to the antigen. Treatments for such hypersensitivity reactions, whether immediate or delayed, often involve desensitization therapy or pharmacological interventions like cortisone to manage symptoms and reduce inflammation.