16B09: Exam Report

Describe the immunology and drug treatment of anaphylaxis

32% of candidates passed this question.

It was expected candidates would detail the process of IgE mediated type I hypersensitivity reaction with some discussion of the mediators (Histamine / tryptase and others) and their consequences. Some detail describing time frame of response and the pre-exposure to Antigen (or a similar Antigen) was expected. Drug treatments would include oxygen and fluids as well as more specific agents such as adrenaline and steroids. Adrenaline is the mainstay of therapy and some comment on its haemodynamic role and prevention of ongoing mast cell degranulation was required.
Better answers noted steroids take time to work and some also discussed the role of histamine blocking agents.

S1i / 16B09: Describe the immunology and drug treatment of anaphylaxis


Anaphylaxis is a life threatening Type I mediated hypersensitivity reaction

NB Anaphylaxis (Gk.  without protection)  – refers to the original theory that the body had used up its protection mechanisms on first exposure and that it was without defence on subsequent exposure to the Ag

Immunology of Anaphylaxis

Trigger: drugs (NMBD), NSAIDs, contrast, latex

Primary Exposure

  • Antigen (Ag) presented by Th cells to B cells
  • B cells activated to become:
    • Memory B cells → live in lymphoid tissue and release specific IgE if Ag represents
    • Plasma Cells → Plasma cells secrete large amounts of IgE into circulation → interact with high-affinite IgE receptors on Mast Cells (MCs) and Basophils ‘priming’ them, this is known as Sensitization
  • No symptoms

Secondary Exposure

  • Ag binds IgE on MCs & Basophils → IgE crosslink → MASS MC degranulation → release of allergenic mediators
  • Memory B cells activated → more IgE coating MCs & degranulation
  • Mediator release is responsible for the anaphylaxis triad; Vasodilatory shock, Angioedema & Bronchoconstriction
  • Mediators:
    • Histamine: increases vascular permeability → angioedema, smooth muscle contraction → bronchoconstriction, relaxation of smooth muscle → vasodilation
    • Bradykinin: production of prostacyclin & NO → mass vasodilation & hypotension. Bradykinin on its own causes itch and increased vascular permeability
    • PGD2: chemotactic for neutrophils, activates eosinophiles
    • Tryptase: activates complement, coagulation & kallikrein-kinin pathways
    • Leukotrienes: trigger sm m contraction of bronchioles
    • Platelet activating factor: platelet activation, aggregation

Drug Tx of Anaphylaxis

Immediate Management

  • Stop exposure to potential triggers
  • Call for help
  • Airway maintenance w 100% FiO2
  • Elevate legs
  • Cardiac arrest? → ALS
  • Adrenaline
  • Fluid Bolus

Secondary Management

  • Antihistamines
  • Steroids
  • Bronchodilators
  • +/- Adrenaline infusion



Mechanism of Action

α1 – vasoconstriction

β1 – positive inotropy

β2 – bronchodilation

β2 – mast cell and basophil stabilisation



Mechanism of Action

Restore circulating volume.  Increase preload and CO



Mechanism of Action

Support respiratory system in setting of severe bronchoconstriction and airway oedema



Mechanism of Action

H1 & H2 antihistamines relieve cutaneous signs and symptoms but have minimal effect on systemic mast cell and basophil degranulation



Mechanism of Action

Improve airway resistance



Mechanism of Action

Glucocorticoids as suppressants of inflammation are used to prevent the late phase of anaphylaxis