Urtikaria, vanliga kent sum búkilska, er ein húðtrupulleiki, sum hevur við sær at tað kemur roði, sum klørnar og er reistur upp.
Patofysiologiin í urtikari hevur við sær, at histamin og aðrir inflammatoriskir mediatorar verða frígivnir frá mastrcellum, sum eru immunceller í húðini og øðrum vevnaði.
Við akuttum urtikaria verður histamin og onnur evni frígivin, tá ið ein fær ovurviðkvæmi fyri ávísum evni, sum t.d. mati, heilivági ella skordýraspjaðing.
Hetta ger, at mastrinafrumurnar avkornast, og tá verður histamin og onnur evni frígivin, sum gera, at blóðæðrarnir leka, og tað gevur ringar.
Hjá kroniskari nátasjúku er orsøkin ofta ókend, men hildið verður, at hon er tengd at eini autoimmunari mekanismu.
Í hesum førinum framleiðir kroppurin sjálvdømi, sum hava sum mál tann høga affinitet IgE receptorin (FcεRI) á mastocytunum, sum førir til aktivatión og útloysn av histamini og øðrum mediatorum.
Bæði í akuttu og kronisku urtikariuni elvir útloysingin av histamini og øðrum mediatorum til eyðkendu sjúkueyðkennini, sum eru kláði, roði og hov.
Viðgerðin fevnir vanliga um at nýta antihistamin fyri at steðga virknaðinum av histamini og minka um sjúkueyðkennini.
Í álvarsligum førum kunnu onnur heilivágur sum kortikosteroid ella omalizumab verða nýtt til at fáa tamarhald á støðuni.
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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['og 6) fysiska ella elektroniska undirskrift hjá rættindahavara ella persóni, sum hevur loyvi at virka fyri rættindahavara.']
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['Set teg í samband við']
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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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