## Type I Hypersensitivity — The Culprit **Key Point:** Type I hypersensitivity is an IgE-mediated, immediate reaction occurring within minutes of antigen exposure, manifesting as urticaria, angioedema, bronchospasm, and potentially anaphylaxis. ### Mechanism The clinical presentation—acute onset within 15 minutes, urticaria, angioedema, and bronchospasm—is pathognomonic for Type I hypersensitivity: 1. **Sensitization phase**: Prior exposure to penicillin → IgE antibodies bind to mast cells and basophils 2. **Re-exposure**: Antigen cross-links IgE → immediate degranulation 3. **Mediator release**: Histamine, tryptase, leukotrienes, prostaglandins → vasodilation, smooth muscle contraction, increased vascular permeability ### Clinical Features of Type I - **Onset**: Seconds to 30 minutes (this case: 15 minutes) - **Manifestations**: Urticaria, angioedema, pruritus, bronchospasm, wheezing, hypotension, anaphylaxis - **Most common cause**: Drug allergy (penicillin, cephalosporins), food allergy, insect venom, latex **High-Yield:** Penicillin is the **single most common drug cause** of Type I hypersensitivity and anaphylaxis in clinical practice. ### Why Not Other Types? - **Type II (cytotoxic)**: Occurs over hours to days; presents with hemolytic anemia, thrombocytopenia, not acute urticaria - **Type III (immune complex)**: Occurs 3–10 days after exposure; presents with serum sickness, vasculitis, arthralgia—not immediate urticaria - **Type IV (delayed-type)**: Occurs 24–72 hours later; presents as contact dermatitis or drug rash—not immediate anaphylaxis **Clinical Pearl:** The **15-minute timeline** is the diagnostic linchpin—only Type I fits this temporal profile. ### Mnemonic for Hypersensitivity Types **ACID**: - **A**ntibody-mediated (Type II) - **C**irculating immune complex (Type III) - **I**mmediate (Type I) - **D**elayed (Type IV)
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