Asthma is a major noncommunicable disease (NCD), affecting both children and adults. Inflammation and narrowing of the small airways in the lungs cause asthma symptoms, which can be any combination of cough, wheeze, shortness of breath and chest tightness.
Asthma affected an estimated 262 million people in 2019 and caused 461000 deaths.
Asthma is the most common chronic disease among children.
Inhaled medication can control asthma symptoms and allow people with asthma to lead a normal, active life.
Causes of asthma
Asthma is now recognized to be a primarily inflammatory condition: inflammation underlying hyperreactivity. An allergic basis can be demonstrated in many adult, and higher percentage of pediatric patients.
In others, a variety of trigger factors (infection, irritants, pollution, exercise, exposure to cold air, psychogenic) may be involved:
Extrinsic asthma: It is mostly episodic, less prone to status asthmaticus.
Intrinsic asthma: It tends to be perennial, status asthmaticus is more common.
Mast cells (present in lungs) and inflammatory cells recruited as a result of the initial reaction produce a multitude of mediators by the following processes:
- Release of mediators stored in granules(immediate): histamine, protease enzymes, TNF-alpha.
- Release of phospholipids from cell membrane followed by mediator synthesis (within minutes): PGs, LTs, PAF.
- Activation of genes followed by protein synthesis (over hours): Interleukins, TNF-alpha.
These mediators together constrict bronchial smooth muscles, cause mucosal edema, hyperemia, and produce viscid secretions, all resulting in reversible airway obstruction.
The inflammation perpetuates itself by cell-to-cell communication and recruitment of more and more inflammatory cells.
Chronic Obstructive Pulmonary Disease (COPD)
Is also an inflammatory disease of the lungs characterized by progressive emphysema (alveolar destruction) and bronchiolar fibrosis in variable proportions.
Loss of bronchiolar elasticity leads to closure of smaller air tubes during expiration. The airways obstruction is accentuated during exercise causing shortness of breath.
Many different factors have been linked to an increased risk of developing asthma, although it is often difficult to find a single, direct cause.
- Asthma is more likely if other family members also have asthma-particularly a close relative, such as a parent or sibling.
- Asthma is more likely in people who have other allergic conditions, such as eczema and rhinitis (hay fever).
- Urbanization is associated with increase asthma prevalence, probably due to multiple lifestyle factors.
- Events in early life affect the developing lungs and can increase the risk of asthma. These include low-birth weight, prematurity, exposure to tobacco smoke and other sources of air pollution, as well as viral respiratory infections.
- Exposure to a range of environmental allergens and irritants are also thought to increase the risk of asthma, including indoor and outdoor air pollution, house dust mites, moulds, and occupational exposure to chemicals, fumes, or dust.
- Children and adults who are overweight or obese are at a greater risk of asthma.
Asthmatic Medication Classification:
- Beta-2 sympathomimetic: Salbutamol, Terbutaline, Ephedrine, others.
- Methylxanthines: Theophylline (anhydrous), Aminophylline and others.
- Anticholinergics: Ipratropium bromide, Tiotropium bromide.
2. Leukotriene antagonists
- Mast cell stabilizers
Sodium cromoglycate, Ketotifen
- Systemic: Hydrocortisone, Prednisolone and others.
- Inhalation: Beclomethasone dipropionate, Budesonide and others.
5. Anti-IgE antibody
Common asthmatic medicines:
A highly selective Beta-2 agonist; cardiac side effects are less prominent. Selectivity is further increased by inhaling the drug. Inhaled salbutamol delivered mostly from pressurized metered dose inhaler produces bronchodilation within 5 minutes and the action lasts for 2-4 hours.
It is, therefore, used to abort and terminates attacks of asthma, butt is not suitable for round-the -clock prophylaxis. Muscle tremors are the dose related side effect. Palpitation, restlessness, nervousness, throat irritation and ankle edema can also occur.
Oral salbutamol acts for 4-5 hours, is longer acting and safer than isoprenaline, but not superior in bronchodilator efficacy.
Its compounds have been extensively used in asthma, but are not considered first line drugs any more. They are used more often in COPD.
Adverse effects are primarily referable to the g.i.t, CNS and CVS. Headache, nervousness and nausea are early symptoms. Children are more liable to develop CNS toxicity.
The irritant property of theophylline is reflected in gastric pain (with oral), rectal inflammation (with suppositories) and pain at site of i.m. injection. Rapid i.v. injection causes precordial pain, syncope and even sudden death-due to marked fall in BP, ventricular arrhythmias or asystole.
Glucocorticoids are not bronchodilators. They benefit by reducing bronchial hyperreactivity, mucosal edema and by suppressing inflammatory response to AG:AB reaction or other trigger stimuli.
Systemic steroid therapy is resorted to in asthma under the following two situations:
- Severe chronic asthma: not controlled by bronchodilators and inhaled steroids, or when there is frequent recurrence of increasing severity; start with prednisolone 20-60 mg (or equivalent) daily; attempt dose reduction after 1-2 weeks of good control and finally try shifting the patient onto an inhaled steroid. Only few patients require long term oral steroid-in them dose should be kept at minimum.
- Status asthmaticus/acute asthma exacerbation: Asthma attack not responding to intensive bronchodilator therapy: start with high dose of a rapidly acting i.v. glucocorticoids (Hydrocortisone) which generally acts in 6-24 hours-shift to oral therapy for 5-7 days and then discontinue abruptly or taper rapidly.
A short course (1-3 week) of oral glucocorticoid may benefit some patients of COPD during an exacerbation.