L13 Asthma

Asthma is an [blank_start]immune[blank_end] dysfunction, an [blank_start]inflammatory[blank_end] response to a non-pathogenic antigen, therefore an atopic or allergic immune response. • Type [blank_start]I & IV[blank_end] hypersensitivity • Antibody – [blank_start]IgE[blank_end] • [blank_start]Cells[blank_end] – T cells, B cells, mast cells, eosinophils • 2 phases – [blank_start]Sensitisation[blank_end] & inflammation

The [blank_start]Atopic March[blank_end] is the relationship between ashtma, atopic dermatitis(AD) and allergic rhinitis(AR) in children. Children with one [blank_start]atopic[blank_end] condition often will also have [blank_start]another[blank_end]. Food [blank_start]allergy[blank_end] also occurs frequently in children with AD or [blank_start]precedes[blank_end] AD.

The first stage of asthma pathology is the [blank_start]sensitisation[blank_end]. A [blank_start]dendritic[blank_end] cell in the lungs encounters an allergen and becomes activated, then travels to a [blank_start]lymph[blank_end] node. T cell activation and [blank_start]proliferation[blank_end] occurs, which releases [blank_start]interleukins[blank_end], and activates B cells. B cells proliferate and release [blank_start]IgE[blank_end] antibodies. The second stage is inflammation. IgE coated/sensitised [blank_start]mast[blank_end] cells and eosinophils in the lungs encounter the allergen and [blank_start]degranulate[blank_end], releasing histamines, proteases, leukotrienes, and prostaglandins which inflame the airways.

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Non-atopic asthma, also known as [blank_start]intrinsic[blank_end] asthma, is asthma [blank_start]without[blank_end] atopy. A skin test will be [blank_start]negative[blank_end]. Commonly in women, and usually in adults. There are some differences (debated); the presence of [blank_start]innate[blank_end] lymphoid cells (ILCs), and [blank_start]less[blank_end] IgE, for example. Neutrophilic asthma is another type. It is usually [blank_start]late[blank_end] onset and [blank_start]more[blank_end] severe, and less reversible. There are some differences; [blank_start]Th17[blank_end] rather than Th2, [blank_start]neutrophils[blank_end] rather than eosinophils. It is corticosteroid [blank_start]insensitive[blank_end]. Occupational asthma is another type.

The pathophysiology of asthma includes inflammation, hyperresponsiveness/bronchoconstriction, oedema, and remodelling. Inflammation is quite complex and impacts [blank_start]treatment[blank_end] decision. Hyperresponsiveness is [blank_start]reversible[blank_end] early on and can be measured. Oedema is due to [blank_start]mucus[blank_end] hypersecretion. Airway remodelling is associated with a progressive, [blank_start]irreversible[blank_end] loss of lung function. It includes the thickening of the [blank_start]basement[blank_end] membrane, fibrosis, airway smooth muscle [blank_start]hypertrophy[blank_end] and hyperplasia, angiogenesis, and mucus gland hyperplasia.

There is a small but significant dose related association with antibiotics in pediatrics and the development of asthma.

There is a dose dependent association between paracetamol use in first year of life and asthma, i.e. paracetamol increases the risk of asthma.

NZ's rate of asthma in the population is:

In conventional asthma treatment and management, we: - Abolish symptoms - [blank_start]Beta agonists[blank_end] (relievers) - Restore best possible airway function - anti-inflammatory drugs ([blank_start]preventers[blank_end]) - Practice allergen [blank_start]avoidance[blank_end]