The Intern At Work: Internal Medicine
An Approach to Anaphylaxis
Jul 12, 2026 · 14 min · 9 segments
Send us Fan Mail In this episode, we discuss an approach to the acute management of anaphylaxis. Written by Dr. Jen Zheng (Internal Medicine…
The Intern At Work: Internal Medicine
Jul 12, 2026 · 14 min · 9 segments
Send us Fan Mail In this episode, we discuss an approach to the acute management of anaphylaxis. Written by Dr. Jen Zheng (Internal Medicine…
Anaphylaxis is a potentially life-threatening mast cell-mediated reaction that can either be IgE or non-IgE mediated.
For IgE-mediated reactions, following a first exposure to an allergen such as peanuts, the immune system produces allergen-specific IgE antibodies.
These IgE antibodies bind to the surface of mast cells, essentially priming them for any future encounters.
On re-exposure, the allergen cross-links to these bound IgE antibodies, triggering mast cell degranulation.
This reaction subsequently releases mediators like histamine, leukotrienes, and prostaglandins.
The release of these mediators produce the symptoms we classically attribute to anaphylaxis.
Histamine drives vasodilation and increased vascular permeability, leading to hypotension and swelling.
Leukotrienes contribute to bronchospasm and mucus production, resulting in wheeze, airway narrowing, and potentially airway collapse.
Non-IgE-mediated reactions can produce symptoms indistinguishable from those of classic anaphylaxis, triggering mast cell degranulation through distinct pathways such as through complement activation, IgG-mediated reactions, or direct receptor activation.
Anaphylaxis is a potentially life-threatening mast cell-mediated reaction that can either be IgE or non-IgE mediated.
For IgE-mediated reactions, following a first exposure to an allergen such as peanuts, the immune system produces allergen-specific IgE antibodies.
These IgE antibodies bind to the surface of mast cells, essentially priming them for any future encounters.
On re-exposure, the allergen cross-links to these bound IgE antibodies, triggering mast cell degranulation.
This reaction subsequently releases mediators like histamine, leukotrienes, and prostaglandins.
The release of these mediators produce the symptoms we classically attribute to anaphylaxis.
Histamine drives vasodilation and increased vascular permeability, leading to hypotension and swelling.
Leukotrienes contribute to bronchospasm and mucus production, resulting in wheeze, airway narrowing, and potentially airway collapse.
Non-IgE-mediated reactions can produce symptoms indistinguishable from those of classic anaphylaxis, triggering mast cell degranulation through distinct pathways such as through complement activation, IgG-mediated reactions, or direct receptor activation.
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