Urticaria

Histamine

Histamine binds to H1 and H2 receptors to cause arteriolar dilation, venous constriction and increased capillary permeability

anaphlyaxis

an acute, potentially lethal, multisystem syndrome resulting from the sudden release of mast cell- and basophil-derived mediators into the circulation -most often immunologic reaction to foods, medications -may be induced through nonimmunologic mechanisms

anticholinergic effects

block the action of the neurotransmitter acetylcholine in the brain

Angioedema

can be caused by the same pathogenic mechanisms as urticaria but pathology is in the dep dermis and subcutaneous tissue and swelling is the major manifestation -commonly affects the face may be painful or burning but not pruritic

H1 antihistamines 2nd generation

cetirizine loratadine fexofenadine

H1 antihistamines 1st generation

diphenhydramine (OTC benadryl) hydroxyzine chlorpheniramine

treatment with 2nd generation H1 antihistamines

ex. loratadine better tolerated and few fewer sedative and anticholinergic effects and may be used in pt intolerant of 1st generation agents

Urticaria

hives vascular reaction of the skin characterized by wheals surrounded by a red halo or flare (erythema) -caused by swelling of upper dermis cardinal symptom is pruritus (itch) up to 20% of population experience urticaria at some point in their lives

causes of acute urticaria

idiopathic (spontaneous disease, unknown cause) infection (upper respiratory, streptococcal infections, helminthes (parasitic worms) food reactions (shellfish, nuts) drug reactions IV administration (blood products, contrast agents)

causes of chronic urticaria

idiopathic: 50% of chronic urticaria physical urticarias: -pressure, cold, heat, water (aquagenic), sunlight (solar), vibration and exercise

Urticaria: clinical findings

lesions occur in minutes, englarge and disappear within hours individual wheals rarely last >12 hours surrounding erythema will blanch with pressure

Urticaria and angioedema

may occur in any location together or indiviudally may be the cutaneous presentation of anaphylaxis so assessment of the respiratory and cardiovascular systems is vital

IgE- mediated food allergy

more like to present with acute urticaria

Dermatographism

most common form of physical urticaria sharply localized edema or wheal within seconds to minutes after the skin as been rubbed affects 2-5% of the population

acute urticaria

new onset <6 weeks

do you need labs to diagnose acute urticaria?

no laboratory testing is driven by associated signs and symptoms (dyspnea, stridor-grating sound)

Non-immunologic urticaria

not dependent on the binding of IgE receptors ex. aspirin may induce histamine release through a pharmalogogic mechanism where its effect on arachidonic acid metabolism causes a release of histamine from mast cells physical stimuli may induce histamine release through direct mast cell degranulation

allergy testing

not routinely performed in patients with chronic urticaria

treatment of urticaria

oral H1 antihistamines are first line treatment for acute and chronic urticaria 1st generation H1 antihistamines are less well tolerated due to sedation 10-50mg hydroxyzine 1-2 hours before bedtime

medication-induced urticaria

penicillin and related antibiotics are common via the IgE-mediated mechanism aspirin is common cause via a non igE-mediated mechanism 30% of chronic urticaria is exacerbated by aspirin/NSAID use DETERGENT IS NOT a cause of urticaria (more likely irritant or allergic contact dermatitis)

chronic urticaria

reccurent (most days) > 6 weeks

cholinergic urticaria (chronic urticaria)

releasing or responding to acetylcholine triggered by heat and emotion diagnosis of pure physical urticaria is made when the sole cause of a patient's urticaria is a physical factor

Urticaria: pathophysiology

the mast cell is the major effector cell in urticaria Immunologic urticaria: antigen binds to IgE on the mast cell surface causing degranulation, which results in release of histamine