A 28-year-old woman presents to the emergency department with acute onset of facial angioedema, urticaria, and dyspnea 15 minutes after receiving intravenous penicillin for a urinary tract infection. She reports a history of similar reactions to cephalosporins. On examination, she is anxious, with wheezing audible on auscultation, blood pressure 88/54 mmHg, and heart rate 118/min. Serum tryptase level is markedly elevated. Which of the following best describes the pathophysiologic mechanism underlying this reaction?
A. Delayed-type hypersensitivity with Th1 cell infiltration and macrophage activation
B. Immune complex deposition in blood vessel walls with complement activation and neutrophil infiltration
C. IgE-mediated mast cell and basophil degranulation with release of preformed and newly synthesized mediators
D. Direct cytotoxic T-cell-mediated destruction of drug-hapten-coated cells
Explanation
Pathophysiologic Mechanism
This patient presents with anaphylaxis, a Type I hypersensitivity reaction characterized by rapid onset (within minutes) of systemic symptoms including angioedema, urticaria, bronchospasm, and cardiovascular collapse.
Mechanism of Type I Hypersensitivity
Key Point
Type I hypersensitivity is IgE-mediated and involves two phases:
1.
Sensitization phase — Initial exposure to antigen (penicillin) leads to Th2 cell activation and B cell production of IgE antibodies, which bind to high-affinity IgE receptors (FcεRI) on mast cells and basophils.
2.
Re-exposure phase — Cross-linking of IgE on mast cell/basophil surface by antigen triggers rapid degranulation with release of:
The markedly elevated serum tryptase is diagnostic for mast cell degranulation and confirms Type I hypersensitivity. Tryptase peaks at 15–30 minutes post-onset and is the most specific marker for anaphylaxis.
High-YieldNEET PG
The rapid onset (15 minutes), cross-reactivity between penicillins and cephalosporins (due to β-lactam ring homology), and presence of systemic symptoms (cutaneous, respiratory, cardiovascular, GI) are hallmark features of IgE-mediated anaphylaxis.
Why This Mechanism Fits
Timing: IgE-mediated reactions occur within minutes (Type I) vs. hours to days (Type III/IV)
Symptoms: Angioedema, urticaria, and bronchospasm result from histamine and leukotriene effects on endothelial permeability and smooth muscle
Hemodynamic collapse: PAF and other mediators cause vasodilation and increased vascular permeability
Tryptase elevation: Specific marker of mast cell/basophil degranulation
Mnemonic
RASH = Rapid onset, Angioedema/urticaria, Systemic (multi-organ), Histamine/mediators → Type I hypersensitivity
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