ASTHMA.pdf

ASTHMA BY DR ODEYEMI DEPARTMENT OF MEDICINE, COLLEGE OF HEALTH SCIENCES, OSUN STATE UNIVERSITY, OSOGBO.  DEFINITION Asthma is a heterogeneous disease, usually characterised by chronic airway inflammation. It is defined by the history of respiratory symptoms...

ASTHMA BY DR ODEYEMI DEPARTMENT OF MEDICINE, COLLEGE OF HEALTH SCIENCES, OSUN STATE UNIVERSITY, OSOGBO.  DEFINITION Asthma is a heterogeneous disease, usually characterised by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation EPIDEMIOLOGY Asthma is a global disease Prevalence vary from country to country and within geographical areas within a country. 5.4% of Nigerians are asthmatic by current estimates Approximately 10–12% of adults and 15% of children affected WHO estimates that 262 million people worldwide had asthma in 2019 and it caused 455,000 deaths. EPIDEMIOLOGY 2 In developing countries where the prevalence of asthma had been much lower, there is a rising prevalence, which is associated with increased urbanization. It can present at any age, with a peak age of 3 years. In childhood it has a male-to-female ratio of 2:1 until puberty when the male-to-female ratio becomes 1:1 CLASSIFICATION Extrinsic – implying a definite external cause Intrinsic – when no causative agent can be identified Extrinsic asthma occurs most frequently in atopic individuals who show positive skin-prick reactions to common inhalant allergens such as dust mite, animal danders, pollens and fungi Intrinsic asthma often starts in middle age (‘late onset’) RISK FACTORS Occurs as a result of interplay between genetic and environmental factors Several risk factors predispose people to asthma and these should be distinguished from triggers, which are environmental factors that worsen asthma in a patient with established disease. RISK FACTORS FOR ASTHMA Host Factors Environmental Factors Genetic predisposition Indoor allergens Atopy Outdoor allergens Airway Occupational hyperresponsiveness sensitizers Obesity Passive smoking Diet Paracetamol RISK FACTORS Atopy is used to describe a group of disorders (such as asthma, allergic rhinitis and atopic dermatitis) that run in families, have characteristic whealing skin reactions to common allergens in the environment and have circulating allergen-specific IgE. RISK FACTORS Some of the environmental factors include; – Early childhood exposure to allergens such as house dust mite, fungal spores, cockroach antigens (indoor) and pollen (outdoor). – Passive smoking (esp. maternal cigarette smoking) – Occupational sensitizers such as e.g. isocyanates, epoxy resins and wood dust ASTHMA TRIGGERS Allergens Upper respiratory tract viral infections Exercise and hyperventilation Cold air Sulfur dioxide and irritant gases Drugs (β blockers, aspirin) Stress Irritants (household sprays, paint fumes) PATHOGENESIS Inhalation of an allergen in a sensitised atopic asthmatic patient results in a bronchoconstriction The inhaled allergen rapidly interacts with mucosal mast cells via an IgE-dependent mechanism, resulting in the release of mediators such as histamine and the cysteinyl leukotrienes which lead to bronchoconstriction. PATHOGENESIS 2 A full spectrum of inflammatory cells, however, are involved in the pathogenesis of asthma. Epithelial and smooth muscle cells are also capable of releasing inflammatory mediators rather than acting solely as passive targets. All of these cells are also involved in the initiation of asthma in non-atopic patients. PATHOGENESIS 3 Eosinophils are characteristically present in increased numbers in the airway. These cells release bioactive lipid mediators and oxygen radicals; their granules also contain toxic basic proteins The number of airway macrophages is also increased in asthma PATHOGENESIS 4 Microvascular leakage is also a feature and may be triggered by many inflammatory mediators. This results in plasma exudation into the lumen of the airways, contributing to mucous plugging, decreased mucociliary clearance, release of kinins and complement fragments and oedema of the airway wall. PATHOGENESIS 5 As a result of the ongoing airway inflammation, therefore, the asthmatic airway wall is thickened by; – oedema, – cellular infiltration, – increased smooth muscle mass and; – hypertrophy of mucus-secreting glands. PATHOGENESIS 6 With increasing severity and chronicity of the disease, remodeling of the airway occurs, leading to; – fibrosis of the airway wall, – fixed narrowing of the airway and; – a reduced response to bronchodilator medication. PATHOGENESIS 7 CLINICAL FEATURES Asthma is characterised by recurrent episodes of exacerbations, attacks or flare-ups. Patients are asymptomatic in between flare-ups. Acute asthma or asthma flare-ups consist of episodes of progressively worsening symptoms and a decrease in lung functions from the patients usual status. Symptoms are usually worse during the night CLINICAL FEATURES 2 Symptoms include; – breathlessness, – cough, – wheeze, and; – chest tightness. The signs include; – agitation, – tachypnoea, and; – tachycardia. CLINICAL FEATURES 3 Use of accessory muscles and inability to talk in sentences or even in phrases may or may not be present, depending on the severity of the flare- up. These signs and symptoms are accompanied by a reduction in lung function as measured by FEV1, Peak expiratory flow rate (PEFR), PaO2, PaCO2, and arterial oxygen saturation (SaO2) CLINICAL FEATURES 4 The severity of these symptoms and signs, along with the findings on functional lung assessment, are used to categorize acute asthma or asthma exacerbations or flare ups as; – Mild; – Moderate; – Severe, – Life-threatening or; – Near fatal ACUTE MILD ASTHMA Breathlessness While walking May be agitated Tachypnoea End expiratory wheeze Peak expiratory flow rate (PEFR) ≥ 70% Prompt relief from SABA (+/- steroid) ACUTE MODERATE ASTHMA Breathless at rest Usually agitated Tachypnoeic Wheezes through out exhalation Pulse rate: 100 – 109b/min Pulsus paradoxus may be present (10-25mm Hg) PEFR 50-69% of best or predicted. Relief from repeated doses of steroid. ACUTE SEVERE ASTHMA Breathless at rest Usually agitated Unable to complete sentences (usually a word at a time) Tachypnoeic with a RR often ≥25c/min Use of accessory muscles of respiration Loud inspiratory and expiratory wheeze Pulse rate ≥110b/min Pulsus paradoxus >25mmHg (only present in 45% of cases) ACUTE SEVERE ASTHMA 2 PEFR