Asthma PDF

Lec: 1 Dr. Mohammed Alhamdany Objective 1- To know the definition of asthma. 2- To identify the causes of asthma. 3- To understand the pathophysiology of asthma. 4- To know the clinical features of asthma. 5- To determine the step...

Lec: 1 Dr. Mohammed Alhamdany Objective 1- To know the definition of asthma. 2- To identify the causes of asthma. 3- To understand the pathophysiology of asthma. 4- To know the clinical features of asthma. 5- To determine the steps in diagnosis of asthma. 6- To know the goals of treatment. Asthma Asthma is a chronic inflammatory disorder of the airways that associated with airway hyper-responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night and in the early morning. These episodes are usually associated with widespread but variable airflow obstruction within the lung that is often reversible, either spontaneously or with treatment. Asthma caused by genetics and environmental factors that include: 1- Indoor and outdoor allergens. 2- Microbial exposure. 3- Diet, vitamins, breastfeeding. 4- Tobacco smoke. 5- Air pollution. 6- Obesity. Pathophysiology Airway hyper-reactivity (AHR): the tendency for airways to narrow excessively in response to triggers that have little or no effect in normal individuals. The relationship between atopy (the propensity to produce IgE) and asthma is well established and in many individuals there is a clear relationship between 1 sensitisation and allergen exposure, as demonstrated by skin-prick reactivity or elevated serum-specific IgE. In cases of NSAID-induced asthma, the ingestion of salicylates results in inhibition of the cyclo-oxygenase enzymes, preferentially shunting the metabolism of arachidonic acid through the lipoxygenase pathway with resultant production of the asthmogenic leukotrienes. Exercise-induced asthma, hyperventilation results in water loss from the pericellular lining fluid of the respiratory mucosa, which, in turn, triggers mediator release. Heat loss from the respiratory mucosa may also be important. With increasing severity and chronicity of the disease, remodeling of the airway may occur, leading to fibrosis of the airway wall, fixed narrowing of the airway and a reduced response to bronchodilator medication. Clinical features Typical symptoms include recurrent episodes of wheezing, chest tightness, breathlessness and cough. Classical precipitants include exercise, particularly in cold weather, exposure to airborne allergens or pollutants, and viral upper respiratory tract infections. Patients with mild intermittent asthma are usually asymptomatic between exacerbations. Individuals with persistent asthma report ongoing breathlessness and wheeze but these are variable, with symptoms fluctuating over the course of one day, or from day to day or month to month. Asthma characteristically displays a diurnal pattern, with symptoms and lung function being worse in the early morning. Cough may be the dominant symptom in some patients, and the lack of wheeze or breathlessness may lead to a delay in reaching the diagnosis of so-called ‘cough- variant asthma’. Some patients with asthma have a similar inflammatory response in the upper airway. Careful enquiry should be made as to a history of sinusitis, sinus headache, a blocked or runny nose and loss of sense of smell. 2 In some circumstances, asthma is triggered by prescription drugs. Beta- adrenoceptor antagonists (β-blockers), even when administered topically as eye drops, may induce bronchospasm, as may aspirin and other non-steroidal anti- inflammatory drugs (NSAIDs). The classical NSAID-induced asthma patient is female and presents in middle age with asthma, rhinosinusitis and nasal polyps. Aspirin-sensitive patients may also report symptoms following alcohol and foods containing salicylates. Other medications implicated include the oral contraceptive pill, cholinergic agents. Diagnosis History Lung function ‘Other’ tests Supportive evidence is provided by the demonstration of variable air- flow obstruction, preferably by using spirometry to measure FEV1 and FVC. This identifies the obstructive defect, defines its severity, and provides a baseline for bronchodilator reversibility. If spirometry is not available, a peak flow meter may be used. Symptomatic patients should be instructed to record peak flow readings after rising in the morning and before retiring in the evening. A diurnal variation in PEF of more than 20% (the lowest values typically being recorded in the morning) is considered diagnostic and the magnitude of variability provides some indication of disease severity. A trial of corticosteroids (e.g. 30 mg daily for 2 weeks) may be useful in establishing the diagnosis, by demonstrating an improvement in either FEV1 or PEF. Exercise tests are useful when symptoms are predominantly related to exercise. Other test: It is not uncommon for patients whose symptoms are suggestive of asthma to have normal lung function. In these circumstances, the demonstration of AHR by challenge tests may be useful to confirm the diagnosis. 3 Measurement of exhaled nitric oxide (FeNO) is a useful test for glucocorticoid- naïve patients as a measure of eosinophilic airways inflammation. An elevated FeNO value supports the diagnosis of asthma and suggests that the patient’s symptoms are highly likely to respond to glucocorticoids. The diagnosis may be supported by the presence of peripheral blood eosinophilia or atopy demonstrated by skin-prick tests or measurement of total and allergen- specific IgE. X-ray appearances are often normal, but lobar collapse may be seen if mucus occludes a large bronchus and, if accompanied by the presence of flitting infiltrates, may suggest that asthma has been complicated by allergic bronchopulmonary aspergillosis. How to make a diagnosis of asthma Compatible clinical history plus either/or: 1- FEV1 ≥12% (and 200 mL) increases following administration of a bronchodilator/ trial of glucocorticoids. 2- >20% diurnal variation on ≥3 days in a week for 2 weeks on PEF diary. 3- FEV1 ≥15% decrease after 6 mins of exercise. Management The goal of asthma therapy is to maintain complete control: “DNA FREE” No daytime symptoms. No nocturnal symptoms/wakening. No limitation of activities. Normal lung function. No need for ‘rescue’ medication. No exacerbations. Avoidance of aggravating factors: 4  Asthma control may be improved by reducing exposure to antigens, for example, household pets. In occupational asthma, removal from the offending agent may lead to cure. Many patients are sensitised to several antigens, making avoidance almost impossible. Patients should be advised not to smoke, as smoking not only encourages sensitization, but also induces a relative corticosteroid resistance in the airway. 5 6 References: Ian D. Penman , Stuart H., et al., editors. Davidson's Principles and Practice of Medicine. 24th ed., Elsevier Health Sciences, 2022. Further information ginasthma.com :Global Initiative for Asthma: comprehensive overview of asthma. brit-thoracic.org.uk :British Thoracic Society: access to guidelines on a range of respiratory conditions. ersnet.org :European Respiratory Society: provides information on education and research, and patient information. thoracic.org :American Thoracic Society: provides information on education and research, and patient information. With best regard 7