asthma
Written by Sarah Lee
Last Reviewed: April 2019
Review Due: April 2020
DEFINITION
‘a chronic inflammatory disease of the airways that is characterised by bronchial hyperresponsiveness and reversible airflow obstruction resulting in recurrent episodes of breathlessness, cough, chest tightness and wheeze that is often made worse by specific triggers’
AETIOLOGY
Complex interactions between genetic and environmental factors are thought to contribute to the development of asthma:
Genetic
Many genes are associated with the condition
A strong family history is very significant
Environmental
Hygiene Hypothesis
Smoking during pregnancy/secondary exposure
Air pollution
Infections
Viral - Rhinovirus, Influenza Virus, Respiratory Syncytial Virus etc
Bacterial - Mycoplasma Pneumoniae, Chlamydia Pneumoniae etc
Allergen Exposure
RISK FACTORS
Family History
Triad of Atopy
History of eczema, atopic dermatitis, allergic rhinitis
Exposure to Allergens
Common Allergens: animal fur, dust mites, pollen, moulds
Occupational Allergens: flour, dusts, chemicals
SIGNS AND SYMPTOMS
Symptoms
Intermittent Dyspnoea
Cough (often nocturnal)
Wheeze
Sputum Production (yellow)
Chest Tightness
Exercise Intolerance
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Signs
Tachypnoea
Widespread wheeze on auscultation
Hyper-resonant percussion
PRECIPITANTS
Cold
Exercise
Stress
Allergens
Respiratory Tract Infections
Drugs (e.g. NSAIDs, Beta Blockers)
Smoking/Passive Smoking
PATTERN OF CLINICAL PRESENTATION
Diurnal Variation - symptoms worse at night/early morning
Worsens in the presence of precipitants, improves when removed
Nocturnal cough
Patients may complain of disturbed sleep and days off school/work
PATHOPHYSIOLOGY
1. Airway Inflammation
Exposure to allergen triggers an IgE-mediated Type 1 hypersensitivity reaction within the lungs.
Mast cell degranulation and production of inflammatory mediators (eg histamine, leukotrines) and cytokines (eg Il-4, IL-5) occurs.
Inflammatory cells including eosinophils migrate to airways produce more mediators, propagating the inflammatory response.
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2. Airway Obstruction
Inflammation causes bronchospasm, mucosal oedema and increased mucus secretion within airways.
Chronic inflammation may cause bronchial smooth muscle hypertrophy and airway remodelling over time which may cause airflow limitations to be only partially reversible.
3. Bronchial Hyperresponsiveness
Eosinophil products increase resting tone of bronchial smooth muscle.
Bronchi become hyperresponsive and produce a larger response, more quickly to the allergen on the next exposure.
Investigations
Spirometry
Gold standard diagnostic test for asthma
Should show an obstructive pattern (i.e. FEV1:FVC <0.7)
Must also show reversibility (at least 15% improvement) after bronchodilator
Peak Expiratory Flow (PEF)
PEF in asthmatic patients is typically lower than expected for the patient's height, age and gender
Monitoring and recording PEF can help establish variability, triggers and efficacy of medicine
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FBC
Normal or Eosinophilia​
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CXR
May show hyperinflation in chronic asthma​
TREATMENT
NON-PHARMACOLOGICAL
Identify and avoid precipitants
Reduce exposure to cigarette smoke
Breathing exercises (physiotherapist-taught)
pharmacological
Guidelines from the British Thoracic Society and Scottish Intercollegiate Guidelines Network suggest the best approach to the long-term management of asthma. They recommend a five-step approach, that can be escalated or de-escalated as guided by the patient's symptoms. Guidelines for the management of asthma in children follow a similar approach.
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Common classes of drugs used in the management of asthma include:
Short Acting Beta2 Agonists/SABA (e.g. Salbutamol)
Long Acting Beta2 Agonists/LABA (e.g. Salmeterol)
Inhaled Corticosteroids (e.g. Beclometasone)
Leukotriene Receptor Antagonists (e.g. Montelukast)
adult

children

EPIDEMIOLOGY
Asthma affects more than 30 million people in Europe with an estimated 8 million (12% of the population) in the UK having a diagnosis of asthma.
REFERENCES
Oxford Handbook of Clinical Medicine (pages 178-182)