The word asthma comes from the Greek word for panting, which is often how patients present. Chronic inflammation of the airways causes narrowing of the airways and therefore more difficult to breathe through, usually triggered by something in the environment.
There are two different types of asthma; genetic asthma, which presents in those less than 12 years old and has a strong family history of asthma. Then there is environmental asthma which presents in people later in life. There are many theories about environmental asthma including the hygiene hypothesis.
Asthma forms part of the atopic triad, which also includes atopic dermatitis and allergic rhinitis. This triad causes an excessive reaction of T helper cells within the immune system. Asthma is usually stimulated by a trigger such as dust or cigarette smoke. When this allergen is present a dendritic cells engulfs it, and presents it to a Th0 cells (undifferentiated T helper cell) which “checks” the allergen. In people without asthma allergens are usually ignored, however in people with asthma the Th0 cell transforms into a Th2, which then activates the humoral immune system. Interleukins are produced especially IL-4 and IL-5. IL-5 stimulates eosinophils to secrete more cytokines and leukotrienes. These damage the epithelium, which over a number of years causes oedema and fibrosis leading to thickening of the basement membrane, reducing the diameter of the lumen. IL-4 stimulated the production of IgE antibody which causes mast cells to produce histamine, leukotrienes and prostaglandins. IgE produces a type 1 hypersensivity reaction. This type of reaction results in the smooth muscle of the bronchioles to spasm and an increase in the mucus secretions, both leading to narrowing of the airways. This narrowing causes the classical wheeze associated with asthma, as the reduced diameter produces a whistle like effect.
During an acute asthma attack there is a range of severities; these can be divided into, mild, moderate, severe and life threatening. The following table shows the clinical features of the different degrees of severity:
(PEF = peak expiratory flow rate – this is as a percentage of what value they can usually get, a device to measure this is shown in the photo)
Treatment for chronic asthma ranges from simple conservative measures with an inhaler as required, some patients can rarely use this, to patient that need to take daily inhalers and tablets and need nebulisers at home in case of severe episodes. Beta-2 agonists are commonly used, short acting are used as required such as salbutamol, and long acting can be used regularly every day to prevent attacks. If you saw our blog posts last week you will remember the beta-adrenergic receptors found in the heart and how these are blocked to reduce the heart rate, with a side effect being blocking the beta-2 receptors in the bronchioles too. These medications for asthma have to opposite effect, instead of blocking the receptors they are agonists, which means that they activate the receptors which results in relaxation and dilation of the bronchioles increasing the diameter of the lumen. Daily corticosteroids are given to some patients in order to dampen the immune response and prevent such as severe reaction to allergens. Leukotriene receptor antagonists can also be used as these decrease bronchoconstriction and inflammation.
Treatment for acute asthma attacks depends on the severity. Some of the basic principles include administering oxygen to maintain O2 saturations, encouraging use of salbutamol inhaler if mild or no nebulised salbutamol available. Steroids are used in all cases of acute asthma attacks. Nebulised ipratropium bromide in those with severe or not responding to initial treatment. IV magnesium sulphate is severe cases or in those that don’t respond to beta agonists.
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