chapter 37: Assessment and management of patients with allergic disorders

Manifestations of anaphylaxis

-Affects multiple organ systems -can be mild, moderate, or severe -the faster the onset, the more severe the reaction -The severity of previous reactions does not determine the severity of subsequent reactions. -Severity depends on the degree of allergy and the dose of allergen exposure.

Hereditary angioedema

-Is a rare, autosomal dominant disorder. -Attacks are precipitated by trauma or spontanously. -Swelling, no itching or urticaria, last 2-4 days and resolve without treatment. Can have severe abdominal pain. -Can be associated with respiratory obstruction and asphyxiation. Treatment: tracheostomy, epinephrine, antihistamines, and corticosteroids.

Anaphylactic (Type I) Hypersensitivity

-Most severe reaction -rapid onset (minutes of exposure to antigen) or delayed reaction may occur and last for up to 24hrs. -characterized by edema in larynx and other areas. -causes hypotension, bronchospasm, cardiovascular collapse -primary chemical mediators are responsible -reaction is local or systemic

Manifestations of severe systemic reactions

-abrupt onset bronchospasm laryngeal edema severe dyspnea cyanosis hypotension dysphagia abdominal cramping vomiting diarrhea seizure cardiac arrest coma flushing warmth anxiety itching peripheral tingling sensation of warmth sensation of fullness in mouth and throat. Nasal congestion periorbital swelling pruritis sneezing tearing of eyes bronchospasm laryngeal

Epicutaneous immunotherapy (EPIT)

-allergen is delivered to the epidermis -do not initiate during pregnancy -failure is evident when pt does not have decrease symptoms within 12-24mos (fails increase tolerance to allergen and fails to use decrease medications to reduce symptoms)

Serum IgE test (RAST)

-an automated test performed on blood samples by pathology lab. -detects free antigen-specific IgE in serum. (not IgE bound to mast cells in skin) -advantage: decreased risk of a systemic reaction, stability of antigen, and lack of dependence on skin reactivity modified by medication disadvantage: limited allergen selection, reduce sensitivity compared with ID skin test, lack of immediate result, higher cost.

Common causes of anaphylaxis

-antibiotics and radiocontrast dye- cause most serious anaphylactic reactions -Penicillin (most common med to cause anaphylaxis) -Foods: peanut, tree nuts, shellfish, fish, milk, eggs, soy, wheat -Medications: sulfa, penicillin, allopurinol, radiocontrast agent, anesthetic agents (lidocaine, procaine), vaccines, hormones (insulin, vasopressin, acth), aspirin, NSAIDs -Animal serum (tetanus antitoxin, snake venom antitoxin, rabies antitoxin), antigen used in skin testing -Insect sting from bees, wasps, hornets, yellow-jackets, ants -Latex

Immune complex (type III) hypersensitivity

-antigen-antibody complexes are cleared from circulation by phagocytes. -deposited in tissue or vascular endothelium -2 factors contribute to injury: increases circulating complex & presence of vasoactive amines -results in vascular permeability and tissue injury

Nursing management of anaphylaxis

-assess for airway, breathing pattern and vital signs. -observe for edema, respiratory distress and prompt notification of the rapid response team and provider. -Document the interventions used and the patient's vital signs and response to treatment.

Pathophysiology of anaphylaxis

-caused by crosslinks of an allergen with allergen-specific IgE antibodies found on mast cells and basophils, leading to cell degranulation. Release of mediators cause activation of platelets, eosinophils, and neutrophils. Histamine, prostaglandins, and inflammatory leukotrienes are potent vasoactive mediateors implicated in vascular permability changes, flushing, urticaria, angioedema, hypotension, and bronchoconstriction that characterize anaphylaxis Smooth muscle spasm, bronchospasm, mucosal edema, inflammation, and increased capillary permeability resutl. Symptoms are sudden in onset and progress in severity over minutes to hours.

Mast cell stabilizers

-cromolyn sodium MOA: stabilizes the mast cell membrane thus reduces the release of histamine and other mediators of allergic response. Also inhibits macrophages, eosinophils, monocytes, and platelets involved in the immune response. -used prophylactically before exposure -benefits may take a week to manifest adverse effects: stinging, burning and sneezing.

skin testing precautions

-do not perform during period of bronchospasm -epicutaneous tests are performed before other testing methods. -emergency equipment must be readily available to treat anaphylaxis.

Allergic rhinitis

-hay fever & allergic rhinitis (seasonal) -Type I hypersensitivity immunologic reaction -symptoms similar to viral rhinitis. -induced by airborne pollens or molds -seasonal occurrence in early spring d/t tree pollen, early summer (grass pollen), and early fall (weed pollen eg ragweed). -attacks begin and end the same time -Histamine is the major mediatorof allergic reaction in the nasal mucosa. -tissue edema results from vasodilation and increased cap permeability -s/s: serous nasal discharge, nasal congestion, sneezing, nose/throat itching. -also post-nasal drip, itching, watery eyes, headache, hyposomnia, and bronchial asthma -diagnostics: nasal smear, blood counts, total serum IgE, epicutaneous and ID testing, nasal provocation test. (false pos and neg responses may occur) Medical management: -avoidance therapy -pharmacologic therapy (1.antihistamines, 2.adrenerics, 3.mast cell stabilizers, 4.corticosteroids, 5.leukotriene modifiers), -Immunotherapy (sublingual, epicutaneous, and subcutaneous). Complications: -anaphylaxis -impaired breathing -non adherence to therapy

Corticosteroids

-indicated in more severe cases of allergic rhinitis; prevents or suppresses major symptoms of allergic rhinitis. -beclomethasone -budesonide -flunisolide -triamcinolone Topical decongestants should be given prior to administration. -full benefit may take effect several days to 2 weeks -adverse effects: drying of nasal mucosa, burning, itching -recommended use is limited to 30days -Immunosuppressant so avoid use in those with TB or bacterial infection -Risk for infection! -oral and parenteral forms are used when conventional tx failed and symptoms are severe and short. Can control hay fever, med-induced allergiies, and allergic reaction to insect stings but not anaphylaxis -Patients who receive high-dose or long-term therapy should not stop taking meds suddenly- adrenal insufficiency! -s/e: fluid retention, weight gain, hypertension, gastric irritation, glucose intolerance, adrenal suppression.

nursing diagnoses: allergic rhinitis

-ineffective breathing pattern r/t allergic reaction -deficient knowledge about allergy -ineffective coping with chronicity of the condition

b-cells

-lymphocyte that produce antibodies -programmed to produce one specific antibody -stimulates plasma cells -results in outpouring of antibodies

nursing interventions: allergic rhinitis

-modify environment -reduce exposure to ppl with upper respiratory tract infections -keep appointments for desensitization procedures -need to know difference b/w meds for allergy exacerbation & seasonal flares (antihistamines) and allergy control throughout the year (corticosteroids, leukotriene modifiers). -assist patient in verbalizing concerns in a supportive environement -evaluate respiratory status, pulse, bp, and cardiovascular status -assist pt in identifying potential barriers and explore acceptable solution for effective management of the condition. -instruct to avoid rubbing or scratching the injection site. -need to continue with the series for the period of time required. -Inform of effects caused by overuse of sympathomimetic agents in nose drops or sprays, because a condition referred to as rhinitis medicamentosa may result. - nasal mucous membranes become more edematous as more medication is used.- NEED TO D/C MEDICATION IMMEDIATELY

Subcutaneous immunotherapy (SIT)

-most common method of treatment Consists of injecting extracts of the allergen that causes symptoms in a patient. -Injections start in small amount and gradually increased until a maximum tolerated dose is obtained. -systemic reaction is rare, but can occur at the up-dosing phase. -patient should be monitored after administration for at least 30mins. -maintenance booster every 2-4 weeks for several years. -epinephrine should be available.

Cytotoxic (Type II) Hypersensitivity

-occurs when system mistakenly identifies a normal constituent of the body as foreign. -associated with myasthenia gravis (antibody against normal nerve ending receptor), Goodpasture syndrome (antibody against lung and kidneys aki)

Medical management of anaphylaxis

-resp and cardiovascular functions are evaluated -oxygen and epinephrine 1:1000 should be administered -most adverse events associated with admin of epinephrine occur when the dose is excessive or given IV. -older pts, those with HTN, arteriopathies or ischemic heart disease are at risk for adverse effects -antihistamines and corticosteroids can be given adjunct to epinephrine (but not in place of). -IV fluids, volume expanders and vasopressor agents given to maintain bp and normal hemodynamic status. -aminoohyline and corticosteroids can be given to improve airway patency and function. -risk of rebound or delayed reaction 4-8 hours after initial allergic reaction.

Prevention of anaphylaxis

-strict avoidance of potential allergens -those allergic to insect stings avoid areas populated by insects, use appropriate clothing and insect repellent -Autoinjector system for epinephrine should be carried. Epipen and Auvi-Q -Allergies should be screened prior to medication being prescribed. -People predisposed to anaphylaxis should wear a medical bracelet or necklace which names allergies. -venom immunotherapy can control (not cure) the systemic reaction. -Desensitization for insulin-allergic patients

Antibodies react to antigens by

1. coating antigen surface if they are particular substances 2. neutralizing antigen if they are toxins 3. Precipitating the antigens out of solution if they are dissolved 4. Prepare the antigens so phagocytes can dispose of them.

Allergy assessment form

1.chief complaint 2.present illness 3. collateral allergic symptoms 4. family allergies 5. previous allergic treatment or testing, prior skin testing, medications 6. physical agents and habits 7. when symptoms occur time, course of illness, time of year, monthly variation, after insect stings 8. where symptoms occur, living, effect of school or work, effect of hospitalization, effect of specific environment, symptoms occur around leaves, hay, lakeside, barn, dry attic, animals 9. what does pt think makes symptoms worse? 10. under what circumstance is pt free of symptoms? 11.summary and additional comments

Cold Urticaria

A condition in which the skin reacts to exposure to cold with localized edema associated with severe itching -FACU (familial atypical cold urticaria)- autosomal dominant and symptoms begin at birth. -ACU (acquired cold urticaria)- affects children and young adults. -hives, lesions that subside in 2 days, fever, chills, conjunctival infection, sweating, headache, and arthralgia. -may develop leukocytosis, increase erythrocyte sed rate (ESR) and raised C-reactive protien level. diagnosed by physical testing with ice cube provocation test. -medical management: avoid cold stimuli bed rest, warmth, corticosteroids -should carry an EpiPen b/c hives can progress to anaphylaxis.

anaphylactoid reaction

A non-IgE-mediated response that causes the rupture of mast cells and basophils, which then release histamine and other defense mediators. -occurs with medications, food, exercise, or cytotoxic antibody transfusion. -local or systemic reaction, involving urticaria and angioedema at site of antigen exposure. -Possibly severe but rarely fatal -treatment identical to anaphylaxis

antibody

A protein that acts against a specific antigen

Contact dermatitis

A type IV hypersensitivity reaction -acute or chronic skin condition caused by contact with an exogenous substance that elicits an immune response. -4 types: 1.allergic 2.irritant 3.phototoxic 4.photo allergic -80% caused by exposure to irritants (soap, detergent, organic solvent) -skin sensitivity may develop after brief or prolonged use. s/s: itching, burning, erythema, skin lesions, edema, skin thickening, hardening, scaling severe response: hemorrhagic bullae diagnostic/assessment: -environmental history- of exposure to contact allergen required to verify diagnosis. patch test- Thin-layer Rapid USe Epicutaneous (TRUE) test Treatment: -avoidance or removal of allergen -Aluminum acetate or cool water compress for allergic CD. -corticosteroids -antihistamines -hydrophilic cream and antibiotics (for infection) for irritant CD.

Immunotherapy

Aka allergy vaccine therapy: involves administration of gradually increasing quantities of allergen until a dose is reached that is effective in reducing disease severity from natural exposure. -used for grass or pollen allergy -reduces IgE, increases IgG -reduces mediator sensitivity -indicated for allergic rhinitis and bronchial asthma -alters disease course in 3-5 years of therapy contraindications: use of beta-blockers or ACE inhibitors, cardiac disease or organ failure, nonadherence to therapy schedule, absence of rescue equipment if reaction occurs.

action of heparin

Anticoagulant

Diagnostic evaluation

CBC with differential Eosinophil count elevated >5-10% Total serum IgE level- high levels support dx of allergic disease. Skin tests- require intradermal or superficial application of solution at several sites. Positive wheal-and-flare. Most accurate confirmation of allergy

mast cells

Connective tissue cells that contain heparin and histamine

antihistamines

H1 Receptor Antagonists (1st Gen) MOA: bind to H1 receptor in CNS and cause sedation • Chlorpheniramine • Diphenhydramine • Hydroxyzine H1 Receptor Antagonists, (2nd Gen) -MOA:do not readily enter the brain & bind to PNS not CNS so it is non-sedating. • Desloratadine • Fexofenadine • Loratadine • Cetirizine • Levocetirizine s/e: drowsiness & dry mouth also: anxiety, agitation, urinary retention, blurred vision, anorexia, nausea, and vomiting. contraindicated: during pregnancy, nursing mothers, newborns, children and older adults, those who have hypersensitivity to drugs for asthma, urinary retention, open-angle glaucoma, hypertension, prostatic hyperplasia)

Food allergy

IgE mediated food allergy Type I hypersensitivity reaction Most common foods: lobster, shrimp, crab, clams, fish, peanuts, tree nuts, berries, eggs, wheat, milk, and chocolate. -Most severe are caused by peanuts and tree nuts. -no evidence that eating while pregnant or lactation affects development of allergies later. -dangerous because they can be hidden in other food -s.s: anaphylaxis, urticaria, dermatitis, wheezing, cough, laryngeal edema, angioedema, GI symptoms: itching, swelling of lips, tongue, palate, abdominal pain, nausea, vomiting, cramps, diarrhea -diagnostics: -allergy history, physcial exam, skin prick test Medical management: elimination of food; H1 blockers, antihistamines, adrenergic agents, corticosteroids, cromolyn Should carry EpiPen nurse teaching: recognizing anaphylactic reaction, should wear medical ID bracelet,

Physiology of IgE-Mediated Allergies

IgE producing cells are in respiratory and intestinal mucosa -2 or more igE molecules bind to an allergen and -> trigger mast cells or basophils to release chemical mediators (e.g. histamine, serotonin, kinins, slow-reacting substance of anaphylaxis, neutrophil factor ->produces allergic skin reaction, asthma, hay fever

secondary mediators

Inactive precursors that are formed or released in in response to primary mediators.

Adrenergics

MOA: vasoconstrictors of mucosal vessels and used topically and opthalmically. Reduces blood flow, fluid exudation, and mucosal edema -Afrin -Alphagan P -pseudoephedrine (Sudafed) should only use a few days to avoid rebound congestion s/e: hypertension, dysrhythmia, palpitation, CNS stimulation, irritability, tremor and tachyphylaxis

specificity

Only specific antigens (key) fit only certain antibodies (locks).

Primary mediators

Performed and stored in mast cells or basophils

avoidance therapy

Remove allergen that act as precipitating factor. Use of air conditioner, air purifier, removal of dust catching carpets, coverings, pets, pillow and mattress cover impermeable to mites and smoke free environment

Delayed-Type (Type IV) Hypersensitivity

T-cell dependent macrophage activation and inflammation cause tissue injury (PPD test for TB)

Dermatitis Medicamentosa (Drug Reactions)

Type 1 hypersensitivity disorder -skin rashes associated with certain medications -leading cause of fatal anaphylaxis -Common with Penicillin, cephalosporin, and sulfonamide antibiotics -NEED TO STOP TAKING IMMEDIATELY & CALL MD -may involve other organs than skin.

Urticaria (hives)

Type I hypersensitive allergic reaction associated with sudden appearance of edematous, pink or red wheals of variable size from 2-4mm and general pruritis -fade within 24-48hrs and the condition resolves in 3 weeks. If >6 weeks it is called chronic urticaria. -management: eliminate drug or food that caused it. avoid use of NSAID avoid heat, stress, alcohol and tight clothes -give antihistamines and corticosteroids

immunoglobulins

a family of closely related proteins capable of acting as antibodies -5 classes: IgG, IgA, IgM, IgD, and IgE -found in lymph nodes, tonsil, appendix, peyer patches, blood, and lymph -igE involved in allergic disorders and parasitic infections

leukotrienes

a group of chemical mediators that initiate the inflammatory response

allergen

a substance that causes an allergic reaction e.g. dust, weeds, pollen, dander can also be called an antigen

bradykinin

a substance that stimulates nerve fibers and causes pain

function of chemical mediators

allergen triggers B-cell to make IgE IgE attaches to mast cell when allergen reappears, it binds to IgE this triggers mast cell to release its chemicals causes symptoms of immediate hypersensitivity

Latex allergy

allergic reaction to natural rubber latex -implicated in rhinitis, conjunctivitis, contact dermatits, urticaria, asthma, and anaphylaxis -risk factors: female, spina bifida, healthcare workers, patients with atopic allergies, multiple surgeries, people in factories that manufacture latex. -Food handled with latex gloves can stimulate an allergic response. -cross reactions for ppl who are allergic to kiwi, banana, pineapple, mango, passion fruit, avocados, and chestnuts. -powder used in gloves can carry latex proteins and when removed or put on, they can be inhaled or settle on surfaces. -s/s: irritant dermatitis erythema and pruritis -hand lotion worsens symptoms -can have a delayed, type IV reaction where symptoms are: vesicular skin lesions, papules, pruritis, edema, erythema, and crusting and thickening of skin. Type I hypersensitivity can include rhinitis, conjunctivitis, asthma, and anaphylaxis. Clinical manifestations: urticaria, wheezing, dyspnea, laryngeal edema, bronchospasm, tachycardia, angioedema, hypotension, and cardiac arrest. -Irritant contact dermatitis is not an allergic reaction to latex. It is the rubbing or other chemical in the glove that causes skin irritation. diagnostic: serum-specific IgE, EIA, or ELISA; skin patch testing (TRUE test); or level of Hevea latex-specific IgE antibody in serum. medical management: avoid latex, antihistamines, epinephrine, medical bracelet, counseled to notify all healthcare workers, paramedics and ambulances. Warning labels can be attached to car windows to alert police & paramedics, may need to d/c work if Type I hypersensitivity Type IV medical management: non-latex gloves, avoid direct contact with latex nursing management: ask all pts about latex allergy, esp those with spina bifida, multiple surgeries. know s/s of latex allergy, promote latex free environment.

Hypersensitivity

an exaggerated response by the immune system to a particular substance

Atopic allergic disorder

asthma allergic rhinitis atopic dermatitis mediated by igE and present together in the same individual and in families

serotonin

chemical mediator that acts as a potent vasoconstrictor and bronchoconstrictor

action of prostaglandins

d and f: bronchoconstriction e: bronchodilation d,e,f: vasodilation smooth muscle contraction increase capillary permeability sensitize pain receptors induce inflammation enhance the effect of inflammatory mediators produce erythema, edema, and heat.

Atopic dermatitis

eczema Type I hypersensitivity disorder d/t genetics, environment, defective function of the skin barrier, and immunologic response. -characterized by inflammation and hyper reactivity of the skin. -chronic pruritis & hyperirritability of the skin -large amounts of histamine on skin -increased serum IgE levels, family history of type I allergies, allergic rhinitis, and asthma. -significant elevation of IgE and eosinophilia (high eosinophils) -excessive dryness of skin, itching, redness, pallor follows in 15-30sec and persist for 1-3mins inflammation result from scratching of erythematous papules. -lesions develop in areas of increased sweating and hypervascularity -atopic march that leads to asthma, allergic rhinitis, or food allergy. Medical management: -avoid contact with the allergen -topical corticosteroids -NSAIDs -antipruritic agents -antibiotics -antihistamines -oral immunosuppressants (cyclosporine, tacrolimus, pimecrolmus) -wear cotton fabrics -wash clothes with mild detergent -humidifying dry heat in winter -avoiding animals, dust, sprays, and perfumes -keep skin moisturized Nursing intervention: instruct the patient and family to be aware of signs of secondary infection & s/e of medication

Manifestations of moderate systemic reactions

flushing warmth anxiety itching peripheral tingling sensation of warmth sensation of fullness in mouth and throat. Nasal congestion periorbital swelling pruritis sneezing tearing of eyes

eosinophil

granular leukocyte

urticaria

hives

allergy

inappropriate and harmful immune system response to substances that are normally harmless

Sublingual therapy (SLIT)

includes a buildup phase followed by treatment plan of 3 times a week with a rapid dissolving tablet or liquid containing allergen extract. -Systemic side effects are rare but reported in pts who also report reactions with SIT. s/e: irritation, minor swelling, itching in mouth, stomach upset, and nausea.

hapten

incomplete antigen

provocative testing

involves direct administration of allergen to the sensitive tissue (conjunctiva, nasal or bronchial mucosa, or GI tract) -identifies clinically significant allergens in pts who have a large number of positive tests. -one antigen per session -risk of producing severe symptoms (bronchospasm in pt with asthma)

angioedema

involves swelling of the deeper layers of the skin -non-pruritic, brawny, non-pitting edema, with well defined margins and erythema similar to urticaria (they can often occur together) -most often involve the lips, eyeslids, cheeks, hands, feet, genitals, and tongue. Mucous membranes of larynx, bronchi, and GI canal may also be affected esp in hereditary type. -can occur suddenly or slowly -ACE inhibitors and penicillin may cause angioedema.

Nonatopic allergic disorder

lack genetic component and organ specificity of atopic disorder -latex allergy

antihistamines + decongestants

loratadine/pseudophedrine cetirizine/pseudophedrine decongestants increase BP so use cautiously in those with hypertension.

T cells

lymphocyte that can: -assist B-cells -stimulate macrophages -destroy target cells -direct flow of cell activity -cause graft rejection -suppress the production of antibodies -Do not bind to free antigens

antihistamine

medication that blocks effects of histamine released by body during allergic reactions

Cytotoxic (Type II) Hypersensitivity

occurs when the system identifies a normal constituent of the body as foreign. Result of a cross-reacting antibody leading to tissue and cell damage. ex: myasthenia gravis, goodpasture syndrome.

Manifestations of mild systemic reactions

peripheral tingling sensation of warmth sensation of fullness in mouth and throat. Nasal congestion periorbital swelling pruritis sneezing tearing of eyes onset of symptoms begins within first 2 hours after exposure

macrophages

phagocytize foreign substances and help activate T cells by (presents antigen to T-cell)

interpretation of skin test results

positive if an urticarial wheal (round, reddened skin elevation), localized erythema (diffuse redness) in the area of inoculation or contact, or pseudopodia (irregular projection at end of wheal) with associated erythema negative= wheal soft with minimal erythema 1+ = wheal 5-8mm with erythema 2+ = wheal 7-10mm with erythema 3+ = wheal 9-15mm with slight pesudopodia 4+ = wheal 12mm+ with pseudopodia and diffuse erythema -false positives may occur because of improper preparation or administration of allergen solution. -corticosteroids and antihistamines suppress skin test reactivity and should be stopped 48-96hrs prior to testing.

types of skin tests

prick test scratch test intradermal testing

anaphylaxis

rapid clinical response to an immediate immunologic reaction between a specific antigen and antibody. -type 1 hypersensitivity -severe life-threatening reaction -rapid release of IgE mediated chemicals

erythema

redness of the skin

photo allergic contact dermatitis

requires light exposure in addition to allergen contact to produce immunologic reactivity. Similar presentation as ACD.

phototoxic Contact Dermatitis

requires sun and chemical in combination to damage epidermis. Similar presentation as ICD.

Allergic contact dermatitis

results from contact of skin and allergenic substance; has a sensitizatin period of 10-14 days presents as vasodilation and perivascular infiltrates on the dermis, intracellular edema on dorsal aspect of hand.

Irritant contact dermatitis

results from contact with a substance that chemically or physically damages the skin on a non-immunologic basis presents as dryness lasting days to months, vesiculation, fissure, cracks on hands and lower arms.

action of leukotrienes

smooth muscle contraction increase vascular permeability bronchial constriction mucus secretion in the airways wheal-and-flare reaction of skin initiates inflammatory response more potent than histamine in causing bronchospasm

action of serotonin

smooth muscle contraction increase vascular permeability potent vasoconstrictor contracts bronchial smooth muscle

action of bradykinin

smooth muscle contraction (bronchi) increase vascular permeability increase mucus production vasodilation hypotension edema stimulates nerves and produces pain

histamine

substance in the body that causes: increased gastric secretion dilation of capillaries constriction of the bronchial smooth muscle

antigen

substance that triggers the production of antibodies; a substance the body recognizes as foreign -2 groups: complete protein antigen (dander, pollen, horse serum) stimulates a complete humoral response & low-molecular-weight substance= haptens that need to bind to tissue or serum protein to produce a carrier complex that initiates an antibody response.

atopy

term often used to describe immunoglobulin E-mediated diseases (i.e., atopic dermatitis, asthma, and allergic rhinitis) with a genetic component

prostaglandins

unsaturated fatty acids that have a wide assortment of biologic activity

action of histamine

vasodilation smooth muscle contraction increased vascular permeability increase mucous secretion -1st to be released in immune and inflammatory response. -stored in high concentration in body -peak in 5-10mins after contact with antigen erythema, edea (wheals), pruritis, bronchocontraction, wheezing, bronchospasm, silates small venules and constric larger vessels, increased secretion of gastic and mucosal cells, result in diarrhea -results from stimulation of H1 & H2 receptors -H1 site of antihistamine action eg diphenhydramine -H2 site of cimetidine and ranitidine action

Leukotriene modifiers

zafirlukast montelukast zileuton MOA: block synthesis or action of leukotrienes and prevent signs and symptoms of asthma. -Long-term use -take medication daily -take in conjuction with inhaled corticosteroid for mild persistent asthma.