## Pathophysiology of Type I Hypersensitivity **Key Point:** The acute onset (15 minutes) of urticaria, angioedema, and stridor following drug exposure is pathognomonic for Type I hypersensitivity (immediate hypersensitivity). ### Mechanism of Type I Hypersensitivity 1. **Sensitization phase** (prior exposure): IgE antibodies bind to high-affinity IgE receptors on mast cells and basophils 2. **Re-exposure phase** (current presentation): Drug-hapten complex cross-links IgE on mast cell surface 3. **Degranulation**: Calcium influx triggers release of preformed mediators (histamine, tryptase, heparin) and newly synthesized mediators (leukotrienes, prostaglandins, PAF) ### Clinical Features of Type I Hypersensitivity | Feature | Timing | Manifestation | |---------|--------|---------------| | Onset | Minutes to 1 hour | Urticaria, angioedema, stridor | | Mediators | Preformed (minutes) | Histamine → vasodilation, increased vascular permeability | | Mediators | Newly synthesized (hours) | Leukotrienes → bronchoconstriction | | Severity | Can progress | Anaphylaxis with hypotension | **High-Yield:** The **cross-reactivity between penicillins and cephalosporins** (25–30% due to shared β-lactam ring) explains the history of cephalosporin reactions. **Clinical Pearl:** Tryptase levels (released from mast cells) peak 15–30 minutes after symptom onset and can be measured to confirm mast cell degranulation in suspected anaphylaxis. **Mnemonic: HISTAMINE** — **H**yperemia, **I**tching, **S**welling, **T**achycardia, **A**ngioedema, **M**uscle spasm (bronchospasm), **I**ncreased vascular permeability, **N**eed epinephrine, **E**mergency management. [cite:Robbins 10e Ch 6]
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