Ti urticaria, a gagangay a maawagan iti panagkagat, ket maysa a sakit ti kudil a mangpataud iti panagkuyegyeg, panagngato, ken panaglablabes ti nalabaga a kudil.
Ti patofisiolohia ti urticaria ramanenna ti pannakairuar ti histamine ken dadduma pay a mangpalaka a mediator manipud kadagiti mast cell, nga isu dagiti selula ti resistensia a masarakan iti kudil ken dadduma a tisyu.
Iti nakaro nga urticaria, ti pannakairuar ti histamine ken dadduma pay a mediator ket gapu iti allergic reaction iti espesipiko nga allergen, kas iti taraon, agas, wenno kagat ti insekto.
Daytoy ti mangpabassit iti bilang dagiti mast cell, a mangiruar iti histamine ken dadduma pay a manglapped iti panagpussuak dagiti urat, isu a tumaud dagiti wheals.
Iti nakaro nga urticaria, masansan a di ammo ti makagapu, ngem maipagarup a mainaig dayta iti mekanismo ti autoimmune.
Iti daytoy a kaso, mangpataud ti bagi kadagiti autoantibody a mangiturong iti high-affinity IgE receptor (FcεRI) kadagiti mast cell, a mangiturong iti panagaktiboda ken ti pannakairuarda iti histamine ken dadduma pay a mediator.
Iti agpada a nakaro ken napaut nga urticaria, ti pannakairuar ti histamine ken dadduma pay a mediator ti mangituggod kadagiti gagangay a sintoma a panaggagatel, panaglabbaga, ken panagletteg.
Ti panangagas gagangay a ramanenna ti panangusar kadagiti antihistamine a manglapped iti epekto ti histamine ken mangkissay kadagiti sintoma.
Kadagiti nakaro a kaso, mabalin a mausar ti dadduma nga agas a kas iti corticosteroid wenno omalizumab tapno makontrol ti kasasaad.
Wahlgren CF: Pathophysiology of itching in urticaria and atopic dermatitis. Allergy. 1992, 47 (2 Pt 1): 65-75.
Raap U, Liekenbröcker T, Wieczorek D, Kapp A, Wedi B: [New therapeutic strategies for the different subtypes of urticaria]. Hautarzt. 2004, 55 (4): 361-6.
[Recommendations for the diagnosis and treatment of urticaria in children]. Arch Argent Pediatr. 2021, 119 (2): S54-S66.
Brzoza Z, Grzeszczak W, Rogala B, Trautsolt W, Moczulski D: Possible contribution of chemokine receptor CCR2 and CCR5 polymorphisms in the pathogenesis of chronic spontaneous autoreactive urticaria. Allergol Immunopathol (Madr). , 42 (4): 302-6.
Sweeney TM, Dexter WW: Cholinergic urticaria in a jogger: ruling out exercise-induced anaphylaxis. Phys Sportsmed. 2003, 31 (6): 32-6.
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What is pathophysiology of urticaria?
Urticaria, commonly known as hives, is a skin condition characterized by the appearance of itchy, raised, red welts (wheals) on the skin.
The pathophysiology of urticaria involves the release of histamine and other inflammatory mediators from mast cells, which are immune cells found in the skin and other tissues.
In acute urticaria, the release of histamine and other mediators is triggered by an allergic reaction to a specific allergen, such as food, medication, or insect sting.
This causes the mast cells to degranulate, releasing histamine and other mediators that cause blood vessels to become leaky, leading to the formation of wheals.
In chronic urticaria, the cause is often unknown, but it is thought to be related to an autoimmune mechanism.
In this case, the body produces autoantibodies that target the high-affinity IgE receptor (FcεRI) on mast cells, leading to their activation and the release of histamine and other mediators.
In both acute and chronic urticaria, the release of histamine and other mediators leads to the characteristic symptoms of itching, redness, and swelling.
Treatment typically involves the use of antihistamines to block the effects of histamine and reduce symptoms.
In severe cases, other medications such as corticosteroids or omalizumab may be used to control the condition.
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