Management of Patients with Allergic Disorders

Allergy

inappropriate or harmful immune response to normally harmless substances (allergens)

Allergic reaction

tissue injury caused by antigen-antibody interaction. Occur when the immune system overreacts to an allergen. Mediated by chemical substances like histamine, serotonin, and kinins released during the reaction.

Complete protein antigens and Incomplete antigens (haptens)

Two main types of Antigens

Complete protein antigens

pollen, animal dander, horse serum → produce full humoral response.

Incomplete antigens (haptens)

certain drugs; combine with proteins to form antigenic complexes.

Sensitization

ccurs when allergens enter via skin, respiratory, or GI tract → body produces specific antibodies.

Primary mediators → preformed and stored in mast cells or basophils.

Secondary mediators → formed or released later in response to primary mediators.

Two types of mediators:

Primary Mediators (preformed)

Immediate effects: vasodilation, edema, bronchoconstriction, inflammation. Histamine, ECF-A, PAF, Prostaglandins, Basophil Kallikrein

Secondary Mediators (newly formed)

Sustained inflammation, pain, bronchospasm, vascular permeability. Leukotrienes, Bradykinin, Serotonin, Heparin

Histamine

first mediator released; causes redness, swelling, itching, and bronchospasm.

Leukotrienes

far more potent than histamine in bronchoconstriction.

Bradykinin & Prostaglandins

cause pain, swelling, and vasodilation.

Serotonin

contributes to bronchial constriction and vascular changes.

Antihistamines

block H1 receptors, reducing allergic symptoms.

H2 blockers

reduce gastric acid secretion

Hypersensitivity

An excessive or abnormal immune response to any stimulus. Occurs after re-exposure to an allergen following sensitization. Can result in tissue injury or disease due to overactive immune mechanisms.

Type I - Anaphylactic (Immediate) Hypersensitivity

IgE-mediated reaction. Immediate onset. On re-exposure, the allergen binds to IgE on mast cells and basophils, releasing chemical mediators (e.g., histamine, leukotrienes).

Type 1 hypersensitivity manifestations

Local: Urticaria, allergic rhinitis, asthma. Systemic: Anaphylaxis

Type II - Cytotoxic Hypersensitivity

IgG or IgM antibodies bind to antigens on cell surfaces or basement membranes, activating complement system → cell destruction (lysis) or tissue damage. An example is Hemolytic transfusion reaction

Type III - Immune Complex-Mediated Hypersensitivity

Antigen-antibody complexes (IgG, IgM) form and deposit in tissues or blood vessel walls. These insoluble complexes trigger inflammation via complement activation and attract neutrophils → tissue injury. Widespread inflammatory damage at deposition sites (e.g., kidneys, joints, lungs) like in Rheumatoid arthritis

Type IV - Delayed (Cell-Mediated) Hypersensitivity

T-cell-mediated (no antibodies involved). Sensitized T lymphocytes respond to antigen exposure and release cytokines, leading to inflammation and tissue damage. Occurs 24-48 hours after exposure (delayed).

Type I: Prepare for emergency interventions (epinephrine, airway support).

Type II & III: Monitor for tissue or organ damage.

Type IV: Manage inflammation and prevent further antigen exposure.

Key Nursing Focus on the 4 Types of Hypersensitivity

CBC with Differential, Eosinophil Count, Total Serum Immunoglobulin E (IgE) Levels, Skin Tests, Provocative Testing, Serum-Specific IgE Test

Diagnostic Evaluation of Allergic Disorders

Prick or Scratch test: Superficial (first step)

Intradermal test: Used after negative prick/scratch tests.

Skin Test methods. Must not be performed during bronchospasm. Emergency equipment must be available. Epicutaneous tests performed before intradermal tests to reduce systemic risk

Atopic Disorders and Nonatopic Disorders

Types of IgE-Mediated Allergic Reactions

Atopic Disorders

Have genetic predisposition to produce IgE in response to harmless inhaled or ingested proteins. Ex. Asthma, Allergic rhinitis

Nonatopic Disorders

Lack the genetic component and organ specificity of the atopic disorders. Can present as: Type I reaction (IgE-mediated anaphylaxis), and Type IV reaction (contact dermatitis)

Anaphylaxis

A severe, life-threatening Type I hypersensitivity reaction between a specific antigen and IgE antibody. Leads to rapid release of chemical mediators (e.g., histamine), causing systemic effects.

Degranulation of cells → Release of histamine, prostaglandins, leukotrienes

Vasodilation and increased capillary permeability → Edema, hypotension

Bronchoconstriction and mucosal edema → Respiratory distress

Cross-linking of allergen-specific IgE on mast cells and basophils results in:

Anaphylactoid Reaction

Mimics anaphylaxis but not IgE-mediated but the treatment is the same. Triggered by non-immune mechanisms (e.g., drugs, food, exercise, transfusions). May be local or systemic

Epinephrine, Antihistamines and Corticosteroids, IV fluids/Vasopressors, Aminophylline

Medications for Anaphylaxis

Epinephrine (1:1000 dilution)

First line and most important drug during anaphylaxis. SQ route or IV infusion if severe. Caution in elderly or those with heart disease or hypertension.

Nursing Management for Anaphylaxis

Assess airway, breathing pattern, vital signs

Monitor for increasing edema or respiratory distress

Activate rapid response team / notify provider

Implement emergency measures:

Allergic Rhinitis (Hay Fever)

The most common form of respiratory allergy, caused by a Type I (immediate) IgE-mediated hypersensitivity reaction. Triggered by airborne allergens such as pollens and molds. IgE binds to mast cells, basophils, and eosinophils in respiratory mucosa

Eosinophilia (↑ eosinophils in nasal tissues)

Key feature of Allergic Rhinitis

Inflammation

Tissue edema

Vasodilation

↑ Capillary permeability

Effects of Histamine release

Clinical Manifestations of Allergic Rhinitis

Sneezing, rhinorrhea (runny nose), nasal itching, conjunctivitis, and nasal obstruction

Management of Allergic Rhinitis

Environmental control measures; Antihistamines, Corticosteroid, Adrenergic agents, mast cell stabilizers, Leukotriene Receptor Antagonists; Allergen Immunotherapy (AIT)

Contact Dermatitis

An inflammatory reaction of the skin caused by direct contact with an external (exogenous) substance.

Irritant Contact Dermatitis (ICD) and Allergic Contact Dermatitis (ACD)

Two main types of contact dermatitis

Irritant Contact Dermatitis (ICD)

nonimmunologic inflammation due to direct chemical or physical damage. Contact with chemical or physical agents that damage skin nonimmunologically; may occur after first exposure or repeated contact. Involves keratinocyte damage rather than immune sensitization.

Allergic Contact Dermatitis (ACD)

immune-mediated delayed (Type IV hypersensitivity) reaction involving T-cell activation. Contact with an allergenic substance; sensitization occurs over 10-14 days.

Allergic Contact Dermatitis Manifestation

Itching, burning, erythema, edema, vesicles, bullae, and oozing at site of contact. Scaling, thickened (lichenified) skin, and pigment changes. Limited to area of exposure.

Irritant Contact Dermatitis Manifestation

Dryness, fissures, cracks, vesicles, Burning, soreness rather than itching, Chronic irritation → thickened, rough skin.

Patch Testing

Standard diagnostic tool for Allergic Contact Dermatitis. Uses TRUE test or extended patch test panel. Contraindicated in acute, widespread dermatitis

Clinical diagnosis; negative patch test

Diagnostic Test for Irritant Contact Dermatitis

Atopic Dermatitis (Eczema)

A chronic, inflammatory allergic skin disorder caused by a combination of genetic susceptibility and environmental triggers. A type I immediate hypersensitivity reaction mediated by IgE antibodies.

asthma, allergic rhinitis, and food allergies

The atopic triad which atopic dermatitis is associated with

Drug Hypersensitivity (Medicamentosa)

adverse immunologic reaction to a medication. Leading cause of fatal anaphylaxis

Immediate Reactions, and delayed reactions

Types of Medicamentosa

Immediate Reactions

Medicamentosa that occurs within 1 hour. IgE-mediated (Type I hypersensitivity) Common examples: anaphylaxis, urticaria, angioedema.

Delayed Reactions

Medicamentosa reaction after 1 hour, often days-weeks. Not IgE-mediated. May be Type II, III, or IV hypersensitivity reactions.

DRESS (drug-induced hypersensitivity syndrome)

Reaction that occurs weeks after continuous drug use. Causes fever, rash, eosinophilia, lymphocytosis, hepatitis, myocarditis. Usually caused by Anticonvulsants, allopurinol

Pseudoallergic Drug Reactions

Mimic allergic reactions but not immune-mediated. Due to mast cell degranulation without IgE involvement.

Pseudoallergic Drug Manifestations

Rash, urticaria, angioedema

Fever, malaise, lymphadenopathy

Respiratory distress (anaphylaxis)

Multiorgan involvement

Mucosal erosions, bullae, necrosis

Pseudoallergic Drug Reaction Management

Assess for history of previous drug reactions

Monitor for early signs of hypersensitivity (rash, itching, dyspnea)

Stop the drug immediately if symptoms appear

Administer emergency medications as ordered

Urticaria (Hives)

A Type I hypersensitivity reaction (IgE-mediated) of the skin. Characterized by sudden appearance of intensely pruritic pink/red wheals (hives) that may merge into large plaques.

Acute urticaria: Lasts <6 weeks, develops within minutes to hours, resolves within 24 hours.

Chronic urticaria: Persists >6 weeks, often recurrent and idiopathic.

Classification of Urticaria

Urticaria manifestations

Itching (pruritus) — often intense, Pink/red wheals or plaques of variable size, Lesions appear and disappear within 24 hours, May occur anywhere on the body

Urticaria management

Eliminate or avoid causative agent; Avoid aggravating factors. Identify and document triggering factors. Monitor airway for angioedema

Angioedema

Allergic reaction involving deeper tissues (subcutaneous and mucosal layers) with diffuse swelling. Often occurs with urticaria, but can occur alone. Can be life-threatening if airway is involved.

Mast Cell-Mediated (Histaminergic) Angioedema, and Bradykinin-Mediated Angioedema

Types of Angioedema

Mast Cell-Mediated (Histaminergic) Angioedema

Caused by allergic reactions with Histamine being the key mediator. Often associated with urticaria, flushing, pruritus, bronchospasm, hypotension (anaphylaxis).

Bradykinin-Mediated Angioedema

Not allergic and not histamine-related. Caused by ACE inhibitors (e.g., captopril) or hereditary C1 esterase inhibitor deficiency. Increases vascular permeability → tissue swelling. Develops slowly (24-36 hours) and resolves in 2-4 days.

Management of Mast Cell-Mediated (Allergic) Angioedema

Epinephrine IM for airway or anaphylaxis symptoms, Second-generation H1 antihistamines, Corticosteroids, oxygen and airway monitoring

Management of Bradykinin-Mediated Angioedema

Stop causative drug (ACE inhibitor). Bradykinin B2 receptor antagonist and Kallikrein inhibitor. Antihistamines and corticosteroids are ineffective

Hereditary Angioedema (HAE)

Rare, potentially life-threatening autosomal dominant genetic disorder. Type of Bradykinin-mediated angioedema due to C1 inhibitor (C1INH) deficiency or dysfunction. Leads to unchecked bradykinin production, causing swelling. Presents as Nonpruritic, diffuse swelling (no urticaria).

Cold Urticaria

Type of physical (inducible) urticaria triggered by exposure to cold (air, water, objects). IgE-mediated atopic reaction where mast cells release histamine.

IgE-mediated (Type I hypersensitivity) — most common and well understood.

Non-IgE-mediated — involves delayed/chronic symptoms, often in the GI tract or skin.

Types of Food Allergy

Oral Allergy Syndrome (OAS)

Also called pollen-food allergy syndrome. Most common IgE-mediated food allergy in adults. Linked with pollen allergies (seasonal allergic rhinitis). Triggered by raw fruits/vegetables, but cooked forms usually safe.

Clinician-supervised oral food challenge

gold standard for diagnosing OAS

Latex Allergy

Allergic reaction to proteins in the sap of the Hevea brasiliensis (rubber tree).