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Anaphylactic shock and its implication for nurses.

L C Green
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Abstract

Anaphylactic shock can strike a patient at any time or place. It is sudden allergic response to an environmental situation, insect venom or medically-prescribed drug. Although some members of the public may present in the Accident and Emergency department with life-threatening symptoms, the situation is often most serious when a drug has been given. The mechanism of anaphylactic shock is discussed in this article as is the first line treatment. The immune system and the character of immunoglobulins are highlighted, and the role of the nurse in an emergency situation is given consideration. Legal implications of any action taken are looked at from the standpoint of litigation.

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AnaphylaxisEmergency NursingHumansImmunoglobulinsJournal ArticleReview

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L C Green. 1998. Anaphylactic shock and its implication for nurses.. https://doi.org/10.1016/s0965-2302(98)90008-x

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Anaphylaxis↗
PubMed2007

Enhanced mast cell activation in mice deficient in the A2b adenosine receptor.

Antigen-mediated cross-linking of IgE bound to mast cells via the high affinity receptor for IgE triggers a signaling cascade that results in the release of intracellular calcium stores, followed by an influx of extracellular calcium. The collective increase in intracellular calcium is critical to the release of the granular contents of the mast cell, which include the mediators of acute anaphylaxis. We show that the sensitivity of the mast cell to antigen-mediated degranulation through this pathway can be dramatically influenced by the A2b adenosine receptor. Loss of this Gs-coupled receptor on mouse bone marrow-derived mast cells results in decreased basal levels of cyclic AMP and an excessive influx of extracellular calcium through store-operated calcium channels following antigen activation. Mice lacking the A2b receptor display increased sensitivity to IgE-mediated anaphylaxis. Collectively, these findings show that the A2b adenosine receptor functions as a critical regulator of signaling pathways within the mast cell, which act in concert to limit the magnitude of mast cell responsiveness when antigen is encountered.

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