Random Dermatology MCQ - Type I Hypersensitivity

A 15-year-old boy with a known peanut allergy accidentally ingests a cookie containing peanuts. Within minutes, he develops generalized urticaria, facial angioedema, wheezing, and hypotension. Which of the following immunoglobulins is primarily responsible for initiating this reaction, and what is the key mechanism of the immediate response?

A) IgE; mast cell degranulation
B) IgG; immune complex deposition
C) IgM; complement activation
D) IgA; neutrophil recruitment
E) IgD; B-cell activation

Correct Answer: A) IgE; mast cell degranulation

Explanation

This is a classic presentation of anaphylaxis, the most severe form of a Type I (immediate) hypersensitivity reaction.

Key Features of Type I Hypersensitivity:

• Timing: Immediate onset, within minutes of exposure to an allergen.

• Clinical Presentation:

  • Cutaneous: Urticaria (hives), angioedema.

  • Respiratory: Wheezing, laryngeal edema.

  • Cardiovascular: Hypotension, tachycardia (anaphylactic shock).

• Mechanism: The reaction is mediated by IgE antibodies bound to the surface of mast cells and basophils.

Pathophysiological Sequence:

1. Sensitization: Upon first exposure to an allergen (e.g., peanut protein), a susceptible individual produces allergen-specific IgE antibodies.

2. IgE Binding: These IgE antibodies bind via their Fc region to high-affinity IgE receptors (FcεRI) on mast cells and basophils.

3. Re-exposure & Activation: Upon subsequent exposure, the allergen cross-links the IgE molecules on the mast cell surface.

4. Mast Cell Degranulation: This cross-linking triggers the mast cell to rapidly release preformed inflammatory mediators from its granules.

5. Immediate Effects: These mediators cause the clinical symptoms:

   • Histamine: Vasodilation, increased vascular permeability (causing wheals, angioedema, hypotension), bronchoconstriction.

   • Tryptase, heparin, chondroitin sulfate.

6. Late-Phase Reaction: Mast cells also synthesize and release newly formed mediators (e.g., leukotrienes, prostaglandins, cytokines), which can perpetuate the inflammation hours later.

Why Not the Other Options?

• (B) IgG; immune complex deposition: Describes Type III hypersensitivity (e.g., serum sickness, lupus nephritis).

• (C) IgM; complement activation: Involved in Type II hypersensitivity (e.g., hemolytic transfusion reactions).

• (D) IgA; neutrophil recruitment: IgA is involved in mucosal immunity. Neutrophil recruitment is prominent in Type III reactions and some Type II.

• (E) IgD; B-cell activation: IgD's primary role is as a membrane-bound receptor on naive B-cells for antigen recognition and activation; it is not involved in hypersensitivity reactions.

Management of Anaphylaxis:

• First-line: Intramuscular epinephrine (adrenaline).

• Supportive: Oxygen, fluids, antihistamines, corticosteroids.

Note: Type I hypersensitivity is also the mechanism behind allergic rhinitis, allergic asthma, and atopic dermatitis (eczema). The key players are IgE, mast cells, and histamine. Skin prick testing for allergies directly measures this IgE-mediated response.