Bronchial asthma

Introduction

This is an obstructive condition in which widely spread narrowing of the respiratory airways can change severity over short period of time, either spontaneously or under treatment, and it isn’t a cardiovascular disease. The symptoms of this disease are wheeze ,chest tightness, cough and shortness of breath, often worse at night .

Classically asthma has 3 characteristics:

  • Air flow limitation which is usually reversible spontaneously or with treatment.
  • Airway hyperresponsiveness to a wide range of stimuli.
  • Bronchial inflammation with T lymphocytes, mast cells, eosinophils, smooth muscle hypertrophy, matrix deposition, mucus plugging and epithelial damage.

The National heart and lung and blood institutes secound expert panel on the management of asthma defined bronchial asthma as ” a chronic inflammatory disorder of the airways in which many and cellular elements play a role, in particular ,mast cells, eosinophils, T lympocytes and epithelial cells.

Prevalence

The prevalence of Asthma increased steadily over the end part of the last century, beginning in the developed and then in the developing world. Present estimates suggest that asthma affects 300 million people worldwide, with a predicted other 100 million people affected by 2025. The socio-economic impact is huge, as poor control leads to days lost from school or work, unscheduled health-care visits and hospital admission. The development and course of the disease, and the response to treatment, are influenced by genetic determinants. The quick rise in prevalence implies that environmental factors are critically important in the development and describing of the disease. Upto now, studies have explored the potential role of indoor and outdoor allergens, microbial exposure, diet, vitamins, breastfeeding, tobacco smoke, air pollution and obesity but no clear consensus has emerged.

As above shows the prevalence of the world, the prevalence in Sri Lanka is described as below.

The study showed on 1872 subjects (45.1% males, 48.8% aged18-45 years) of which 12.2% were current smokers. In the total population in Sri Lanka, the prevalence of current wheeze was 23.9% (95% CI: 22.0%-25.9%), of self-reported asthma was 11.8% (95% CI: 10.3%13.2%) and of current asthma medication use was 11.1% (95% CI: 9.6%12.5%). The prevalence of asthma according to a positive response to either of the above questions was 31.4% (95% CI: 29.3%-33.4%) Prevalence of symptoms was higher in adults aged >45 years. Of those with current wheeze, 60.9% denied a diagnosis of asthma and only 38.2% admitted to use of asthmathetic medication. In those with current wheeze, wheezing was the only symptom in 19.9% whereas 80.1% had at least one other respiratory symptom (tightness of chest, cough or shortness of breath) of which cough was the most common symptom. In those without current wheeze, self-reported asthma and current asthma medication use, 30%, 35.9% and 36.6% respectively had at least one other respiratory symptom.

Global statistics tells that there are over 334 million asthmatic patients in the world, with most of these sufferers being from low and middle-income countries like Sri Lanka. And in 2014, Sri Lanka was also listed as one of the countries with no national strategy plan for managing asthma.

So that in the last ten years, the number of asthma cases in the country has increased by a whopping 50%. There have been studies in Sri Lanka showing that children living in unplanned, busy cities have a higher opportunity of having lifetime wheezing than those in planned, cleaner cities.

Another factor that worsen the situation is the fact that people often neglect their medication. Adults seem to shy away from treatment, while parents of asthmatic children often promote misconceptions about the use of inhalers, resulting in poor compliance of inhaled medication. The latter is especially true to low-income families who are unfamiliar with asthma and its treatment. So the prevalence of asthma in Sri Lankan adults is high in comparison with global data.

Catergorization

Clinical diagnosis of Asthma is not, however, always easy, since no single criterion has been identified. For the practical purposes 2 types may be recognized but there is considerable overlap on these two.

  • Extrinsic Asthma, or atopic, asthma is a component of the atopic state, and is therefore a related with atopic eczema and hay fever either in the same individual or in the family. It usually begins in childhood, and is mediated by IgE antibodies against inhaled antigens such as pollens, animal danders, and house dust containing mite antigens, particularly of the genus DERMATOPHAGOIDES. Exposure to such antigens during childhood may cause the disease.
  • Intrinsic Asthma, this type of asthma isn’t related to atopy, but occurs in latter stages of life and may be a complication of chronic bronchitis. Hypersensitivity to bacterial products is predicted but not proven yet. Hypersensitivity to drugs, particularly aspirin (NSAIDs) ,is sometimes a reason. Once the asthma has become established there is a hyperactivity of the bronchi, and any stimulus may cause an attack.

Pathogenesis

The pathophysiology of asthma involves a genetic(atopy) predeposition coupled with environmental factors

Atopic Asthma

Nonatopic asthma-The 2nd largest group of nonatopic or nonreagenic, variety of asthma, which is most frequently triggered by respiratory tract infection.Viruses cause more than bacteria.A positive family is not common, serum IgE levels are normal, and there are no other associated allergies.It is believed that virus induced inflammation of the respiratory mucosa lowers the threshold of the vagal receptors to irritants. Inhaled air pollutants such as SO2, O3 and NO2, may also contribute to the chronic airway inflammation and hyperreactivity that are present in some situations.

Occupational Asthma-It is because of hypersensitivity to an agent inhaled at work. Inhaled agents may act as non specific stimuli precipitating an asthmatic attack in those with hyper-reactive airways, or they may act as agents capable of including asthma and airway hyper-reactivity . Many different occupationally inhaled agents are there which cause asthma. A combination of type 1 and type 3 hypersensitivity is thought to be as the mechanism.

In the country united kingdom, if the asthma can be proved to be a result of an agent inhaled during work, the patient is entitled to statutory compensation.

Drug induced Asthma- NSAIDs, particularly aspirin and propionic acid derivatives ,e.g indometacin, have a major cause in the development and precipitation of attacks in approximately 5% of patients with asthma. This effect of NSAIDs is especially prevalent in those individuals who have both nasal polyps and asthma. It is onsidered that treatment with these drugs leads to an imbalance in the metabolism of arachidonic acid. NSAIDs inhibit arachidonic acid metabolism through the cyclo oxygenase (COX)pathway, by preventing the synthesis of prostaglandins. It is considered that under these circumstances there is a reduced production of prostaglandin E2 which, in a sub-proportion of genetically susceptible subjects, induces the overproduction of cysteinyl leukotrienes by eosinophils, mast cells and macrophages. Patients in that situation there is evidence for polymorphisms involving the promoter region of the LTC4 synthase gene which controls the level of activity of this terminal enzyme of the leukotriene-generating pathway.

Beta-blockers, the airways have a direct parasympathetic innervation that cause bronchoconstriction. There isn’t any direct sympathetic innervations of the smooth muscle of the bronchi, and antagonism of parasympathetically induced bronchoconstriction is only dependent upon circulating epinephrine (adrenaline) acting through (32-receptorson the surface of smooth muscle cells. Inhibition of this effect by beta adrenoreceptor-blocking drugs like as propranol leads to bronchoconstriction and airflow decreasement, but only in asthmatic patients. The so-called selective beta1 adrenergic blocking drugs such as atenolol may still induce attacks of asthma; their use to treat hypertension or angina in asthmatic patients is best avoided.

Non-specific factors for pathogenesis

Characteristic feature of bronchial hyperresponsiveness in asthma means that, as well as reacting to specific antigens, the airways will also respond to a wide variety of non-specific direct and indirect stimuli.

Because of cold air and exercise most asthmatic patients wheeze after prolonged exercise. Typically, the attack doesn’t occur while exercising but afterwards. The inhalation of cold, dry air also precipitate an attack. Exercise -induced wheeze is because of histamine and leukotrienes which are released from mast cells when the epithelial lining fluid of the bronchi becomes hyperosmolar becoming to drying and cooling during exercise. The process can be shown by exercise, cold air and hypertonic (e.g. saline or mannitol) provocation tests.

In considering the diet, increased in takes of fresh fruit and vegetables has been shown to be 0protective, possibly to the increasement intake of antioxidants. Variation of the genetics in antioxidant enzymes is associated with more severe asthma.

Emotion is a well known factors that may influence asthma, but there is no evidence that patients with the disease are anymore psychologically disturbed than their non-asthmatic friends.

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