Hypersensitivity Types Overview

Hypersensitivity Types

• Hypersensitivity reactions are overreactions of the immune system to antigens.
• Five types exist, each with unique pathophysiology, symptoms, and treatments.

Type I: Immediate Hypersensitivity

• Mechanism: IgE-mediated rapid allergic response. Initial exposure creates IgE antibodies which bind to mast cells. Re-exposure triggers mast cell degranulation, releasing mediators (histamine, prostaglandins, leukotrienes).
• Effects: Smooth muscle contraction, vasodilation, bronchoconstriction, increased vascular permeability causing allergic symptoms.
• Epidemiology: Allergic rhinitis affects ~11% U.S. population. Anaphylaxis (most severe) has a 1-2% lifetime prevalence, increasing in children.
• Common Triggers: Food, medications, insect stings, latex.
• Local Reactions (e.g., allergic rhinitis): Sneezing, nasal discharge, sinus pressure, itchy/watery eyes.
• Systemic Reactions (e.g., anaphylaxis): Dyspnea, wheezing, rash, nausea, vomiting, hypotension, tachycardia, angioedema. Severe cases lead to bronchospasm, airway obstruction, anaphylactic shock.
• Management: Mild cases use antihistamines & decongestants. Severe reactions require immediate IM epinephrine (relaxes bronchioles, constricts vessels), oxygen, corticosteroids (e.g., methylprednisolone), and bronchodilators (e.g., albuterol). Nursing care involves monitoring, removing allergen, administering meds, and teaching about EpiPen use and avoidance.

Type II: Cytotoxic Hypersensitivity

• Mechanism: Antibody-mediated; IgG and IgM antibodies target cells, activating complement or antibody-dependent cytotoxicity, leading to cell lysis or dysfunction.
• Examples:
  • Blood transfusion reactions (mismatched blood): hemolysis, acute renal failure, systemic inflammation.
  • Goodpasture's syndrome: autoimmune attack on lung and kidney basement membranes, leading to glomerulonephritis and pulmonary hemorrhage.
  • Myasthenia gravis: autoantibodies bind to acetylcholine receptors, impairing neuromuscular function and causing muscle weakness.
• Management: Remove causative agent (e.g., discontinue mismatched blood). Plasmapheresis (removes harmful antibodies). Corticosteroids, immunosuppressants, sometimes dialysis or renal transplantation (for Goodpasture's syndrome).

Type III: Immune Complex Hypersensitivity

• Mechanism: Antigen-antibody complexes deposit in tissues, causing inflammation and tissue damage. Immune complexes are slow to clear.
• Examples:
  • Systemic lupus erythematosus (SLE): Autoimmune complexes lodge in organs, causing inflammation (vasculitis, nephritis, arthritis, neurological issues).
  • Rheumatoid arthritis (RA): Complexes in joints leading to chronic inflammation and destruction.
  • Serum sickness: Reaction to proteins (in medications or antiserum), causing fever, rash, joint pain, angioedema.
• Management: Remove causative agent. Symptomatic relief with antihistamines, corticosteroids. Severe cases may need epinephrine or immunosuppressants.

Type IV: Delayed-Type Hypersensitivity

• Mechanism: T-lymphocyte mediated, not antibody-mediated. Delayed response (24-72 hours after exposure). Involves macrophage activation and tissue destruction.
• Examples:
  • Contact dermatitis (poison ivy, latex): localized redness, itching, swelling.
  • Mantoux test (Tuberculosis): localized wheal and flare reaction.
  • Latex allergy: Delayed reaction, or sometimes immediate (Type I).
• Management: Prevent exposure. Mild reactions use antihistamines or topical corticosteroids. Severe reactions may need epinephrine, oxygen, IV corticosteroids. Patient education (latex-free precautions, EpiPen).

Type V: Stimulatory Hypersensitivity

• Mechanism: Autoantibodies excessively stimulate cell-surface receptors, leading to overactive cell function.
• Example: Graves' disease: autoantibodies bind to TSH receptors, increasing thyroid hormone production (causing hyperthyroidism: tachycardia, weight loss, heat intolerance).
• Management: Medications to block hormone production (e.g., antithyroid drugs), supportive care for hyperthyroid symptoms.

Nursing Care & Interventions

• General Focus: Prompt recognition, removal of offending agent, prevention of complications.
• Key Interventions:
  • Monitoring: Respiratory status, vital signs, and systemic reaction symptoms.
  • Emergency Preparedness: Immediate access to emergency medications (e.g., epinephrine, corticosteroids), resuscitation equipment.
  • Education: Teach patients to recognize early symptoms, avoid triggers, use EpiPens (if applicable), and wear Medic Alert bracelets.

Conclusion

• Hypersensitivity reactions range from mild allergies to life-threatening anaphylaxis.
• Effective management depends on understanding pathophysiology, prompt intervention, and prevention strategies, tailored to individual needs.
• Nursing care is crucial for monitoring, treatment and education.