Anaphylaxis Flashcards
What is anaphylaxis?
a severe, life-threatening, generalised or systemic hypersensitivity reaction.
What is the pathophysiology of anaphylaxis?
- Caused by a severe type 1 hypersensitivity reaction.
- Immunoglobulin E (IgE) stimulates mast cells to rapidly release histamine and other pro-inflammatory chemicals AKA mast cell degranulation.
- This causes a rapid onset of symptoms, with airway, breathing and/or circulation compromise.
What are the two phases in the pathophysiology of anaphylaxis?
Sensitisation and Effector phase
What is the sensitisation phase of anaphylaxis?
During the initial exposure to an allergen, antigen-presenting cells (APCs) process and present the allergen to naïve T cells, which differentiate into allergen-specific T helper 2 (Th2) cells.
Th2 cells release cytokines, such as interleukin-4 (IL-4) and IL-13, promoting the production of allergen-specific IgE antibodies by B cells.
The IgE antibodies bind to high-affinity receptors (FcεRI) on the surface of mast cells and basophils, sensitizing these cells for future allergen exposure.
What is the effector phase of anaphylaxis?
Upon subsequent exposure to the same allergen, the allergen cross-links the IgE molecules on the surface of mast cells and basophils, triggering the release of preformed and newly synthesized inflammatory mediators.
What are preformed mediators in anaphylaxis?
Histamine, tryptase, and chymase are stored in granules within mast cells and basophils and are rapidly released upon activation.
These mediators cause vasodilation, increased vascular permeability, smooth muscle contraction, and mucus secretion, leading to the clinical manifestations of anaphylaxis.
What are newly synthesised mediators in anaphylaxis?
Following activation, mast cells and basophils synthesize and release various cytokines, chemokines, and lipid mediators, such as prostaglandins and leukotrienes.
These mediators contribute to the late-phase response, amplifying and prolonging the inflammatory process.
What is Non-IgE-mediated anaphylaxis?
Although less common, non-IgE-mediated mechanisms can also contribute to anaphylaxis.
These include complement activation, direct mast cell activation by agents such as radiocontrast media or opioids, and IgG- or IgA-mediated immune complex formation.
What are common identified causes of anaphylaxis?
- Food (e.g. nuts, shellfish, fish, milk, eggs) - the most common cause in children
- Drugs - penicillin and other abx, NSAIDs, chemotherapy
- Venom (e.g. wasp, bees, fire ants)
- Latex - natural rubber latex
- Idiopathic
What does the Resus council define anaphylaxis as?
Sudden onset and rapid progression of symptoms
Airway and/or Breathing and/or Circulation problems
Airway problems may include:
- swelling of the throat and tongue →hoarse voice and stridor
Breathing problems may include:
- respiratory wheeze
- dyspnoea
Circulation problems may include:
- hypotension
- tachycardia
What does it mean if there are no ABC problems?
the patient is technically not having anaphylaxis
What differentiates an anaphylactic reaction from a non-anaphylactic reaction?
compromise of the airway, breathing or circulation.
What do around 80-90% of patients have?
- Skin and mucosal changes
- generalised pruritus
- widespread erythematous or urticarial rash
How does a patient with an anaphylactic reaction present?
- Hx of exposure to an allergen (although it can be idiopathic).
Rapid onset of allergic symptoms:
- Urticaria
- Itching
- Angio-oedema, with swelling around lips and eyes
- Abdominal pain
What additional symptoms may indicate anaphylaxis?
- SOB
- Wheeze
- Swelling of the larynx, causing stridor
- Tachycardia
- Lightheadedness
- Collapse