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Asthma (Clinical Presentation (Episodic shortness of breath, During attack…
Asthma
Clinical Presentation
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During attack - reduced chest expansion, prolonged expiratory time, bilateral expiratory polyphonic wheezes, tachypnoea
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Uncontrolled asthma - PEFR less than 50%, resp rate less than 25, pulse less than 110, normal speech
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Severe attack - inability to complete sentences, pulse greater than 110bpm, respiratory rate greater than 25/min
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Life threatening attack - silent chest, confusion & exhaustion, cyanosis, bradycardia, PEFR less than 33%
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Diagnosis
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Exhaled nitric oxide - measure of eosinophilic inflammation and an index of corticosteroid response - used to assess the efficacy of corticosteroids
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Blood & sputum tests - patients sometimes have increased numbers of eosinophils in peripheral blood but sputum eosinophilia is MORE SPECIFIC FINDING for asthma
Lung function tests
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Peak expiratory flow rate (PEFR) - measurement on waking, prior to taking a bronchodilator and before bed, after a bronchodilator
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Asthma control test - 25: well controlled, 20-24: on target, less than 20: off target
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RCP3 questions - recent nocturnal waking? usual asthma symptoms in day? interference with activity of daily living?
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Treatment
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Other agents with bronchodilator activity e.g. leukotriene receptor antagonist, oral corticosteroids for those not on inhalers
Bronchodilators e.g. beta-2 agonists, muscarinic antagonists, methylxanthines
Steroid-sparing agents - methotrexate, ciclosporin, IV immunoglobulin, anti-IgE monoclonal antibody
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Guidline medication regime
- SABA = mild
- SABA + ICS
- SABA + LABA + ICS
- SABA + LABA + ICS + 4th drug = severe
Aims - abolish symptoms, restore normal or best possible lung function, reduce risk of severe attacks, enable normal growth to occur in children
Epidemiology
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Genetic factors - several genes in combination with environmental factors. These genes control the production of certain cytokines
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Environmental factors - early childhood exposure to allergens and maternal smoking has a major influence on IgE production
Commonly starts in childhood between ages 3-5 years and may either worsen or improve during adolescence
Three characteristics
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Bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation, oedema, smooth muscle hypertrophy, mucus plugging and epithelial damage
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Pathophysiology
Inflammation cause due to mast cells, eosinophils and dendritic cells & lymphocytes
There is changes in the lung after allergen challenge, such as bronchoconstriction and worsening inflammation
Primary abnormality is narrowing of airway due to smooth muscle contraction, thickening of airway wall and inflammation
Precipitating factors - occupational sensitisers such as wood dust, cold air & exercise, atmospheric pollution and irritant dusts, diet, emotion, drugs and allergen induced asthma
Remodelling - a characteristic feature of chronic asthma is alteration of the structure and functions of the formed elements of the airways
Key Facts
Two main types
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Non-allergic/non-eosinophilic (30%) - exercise, cold air & stress, smoking & non-smoking associated, obesity associated
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Differential Diagnosis
Pulmonary oedema, COPD (may co-exist), large airway obstruction caused by foreign body/tumour, pneumothorax, bronchiectasis