Sedating antihistamines asthma

Identifying these severe features aids clinical diagnosis.

Difficulty arises in the interpretation of the symptoms and signs.

The combined physiological effects of these mediators contribute to a multi-organ 'hypovolaemic-distributiveÓshock,whichinvolves: ¤ Smooth muscle contraction, leading to bronchoconstriction and abdominal cramps ¤ Vasodilatation, leading to flushing, urticaria, hypotension and a reduced level of consciousness ¤ Increased capillary permeability, leading to angio-oedema and laryngeal oedema ¤ Activation of vagal pathways, leading to bradycardia and neurocardiogenic syncope.

The rapidity of onset of the severe symptoms and their presentation differ, depending on the causal agent.

If treated inappropriately, or not treated at all, it may, in rare cases, prove fatal.

Rapid diagnosis is essential and dependent on clinical recognition alone.

However, evidence suggests that adrenaline auto-injectors are under-used in severe reactions, related in part to a reluctance to prescribe them.

From an immunological perspective, anaphylaxis can be defined as an immediate systemic reaction caused by the rapid release of potent mediators from tissue mast cells and peripheral basophils (AAAI, 1998).The clinical syndrome of anaphylaxis may involve cutaneous, respiratory, cardiovascular or gastrointestinal symptoms and signs (Figure 1). The constellation and complexity of symptoms of anaphylaxis requiring rapid interpretation.These may also be complicated by panic or fainting.Allergen-driven cross-linking of receptor-bound Ig E activates mast cells and basophils, to release their mediators (Figure 2) (Galli et al, 2005). Activation of mast cells in response to allergens (Galli et al, 2005).Anaphylaxis can be provoked by numerous agents, or allergens, most usefully categorised into drug or non-drug causes (Table 1).

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