Introduction of Asthma

By: Pharma Tips | Views: 2676 | Date: 03-Jul-2011

Asthma is a complex chronic inflammatory disease of the airways that involves the activation of many inflammatory and structural cells, all of which release inflammatory mediators that result in the typical pathophysiological changes of asthma.


Asthma is a complex chronic inflammatory disease of the airways that involves the activation of many inflammatory and structural cells, all of which release inflammatory mediators that result in the typical pathophysiological changes of asthma.


Affects 10% of children & 5%-7% adults
Highest in NZ, Low in Fiji ~ 1%


Asthma is “all in the mind.”
You will “grow out of it.”
Asthma can be cured,
Not very serious disease and nobody dies from it.
You are likely to develop asthma if someone in your family has it.
You can “catch” asthma from someone else who has it.
Moving to a different location can cure asthma.
People with asthma should not exercise.
Asthma does not require medical treatment.
Medications used to treat asthma are habit-forming.
Someone with asthma can provoke episodes anytime.
Asthma can spread to other persons through coughing.
Asthma is born with you. Familial/genetic. (2)


Inhaled allergens - e.g. house dust mite, moulds, feathers, pollen, pet hair,
Food allergies/sensitivities - commonly cow’s milk, eggs, wheat, food additives, cheese, yeast, fish, salicylates (present in many fruits, vegetables, herbs and spices).

Specific foods - not allergy related, e.g. salt, sugar, and alcohol.
Low stomach acid - which favors the development of food allergies.
Immune system challenges - e.g. antibiotics, steroids, amalgam fillings, and candidiasis and childhood vaccinations. Asthma is twice as prevalent in children vaccinated with the DTP vaccine - diphtheria, tetanus and pertussis (whooping cough), or tetanus vaccine alone than in those who are not.
Medicines -e.g. aspirin, non-steroidal anti-inflammatory drugs (NSAIDs), beta-blockers.
Changes in the weather - especially cold air.
Hormonal changes    
Emotional stress, Exercise.


The first step to successful prevention of asthma is to recognize the general symptoms of asthma caused by exposure to triggers. Sometimes the symptoms are so evident that a rapid asthma diagnosis can be made. The most common symptoms of asthma are:
Tightness of the chest (often painless)
Wheezing (loudness varies from almost inaudible to very loud)
Sweating, increased pulse rate and anxiety (more pronounced in severe cases)
Bluish tint (cyanosis) to face, lips, mucous membranes (gums), and nail beds in acute attacks
Cough (due to the accumulation of phlegm/mucus in the lungs).


Mechanisms by which asthma causes airway inflammation and constriction are complex and involve a cascade of events that leads to the release of inflammatory mediators. In extrinsic asthma, this appears to be linked to a change in the ratios of different kinds of lymphocytes in the airway mucosa in favour of those kinds that produce inflammatory leukotrienes and cytokines, which in turn step up IgE production and the activation of mast cells, eosinophils.(2,3,4)

Intrinsic asthma involves disruption of the autonomic nervous system as a result of various triggers. Normally, the actions of the sympathetic and parasympathetic nervous systems are balanced and integrated by the hypothalamus. Intrinsic asthma triggers cause a shift in favour of the parasympathetic nervous system, which leads to airway constriction, mucus production and increased heart rate.

The term bronchial hyper-responsiveness (or hyper-reactivity) refers to abnormal sensitivity to a wide range of stimuli such as irritant chemicals, cold air, stimulant drugs and so on. Stimuli, which cause the actual asthma attacks, are many and various, and include allergens (in sensitized individuals), exercise (in which the stimulus may be cold air), respiratory infections and atmospheric pollutants such as sulfur dioxide. In many subjects the asthmatic attack consists of two main phases as can be demonstrated by tests of FEV: (forced expired vol. in 1 sec.)



The immediate phase, i.e. the initial response, occurs abruptly and is due mainly to spasm of the bronchial smooth muscle. The cells involved in this phase are predominantly mast cells (activated to release histamine, in the case of allergic asthma, by interaction of allergen with cell-fixed IgE). Both platelets and macrophages have receptors for IgE, albeit of low affinity, and there is clinical evidence of platelet activation in vivo during allergic bronchospasm. It is possible that in non allergic asthma, irritants may stimulate the irritant receptors and cause release of peptide mediators by antidromic impulses in sensory nerve fibers, and that these mediators then activate mast cells and other cells. Exercise induced asthma appears to involve only the phenomena of this first phase.


The second, late-phase response, i.e. the delayed response, occurs at a variable time after exposure to the eliciting stimulus and may be nocturnal.

There is usually a blood eosinophilia and also some degree of loss of bronchial epithelium. In view of the increasing evidence for the seminal role of the eosinophils and the epithelial loss, some authorities have stated that asthma should be redefined as 'chronic, desquamating eosinophilic bronchiolitis.

There are two categories of anti-asthmatic drugs: bronchodilators drugs and anti inflammatory agents. Bronchodilators are effective in reversing the immediate response, antiinflammatoryagentsininhibitingorpreventing the later phase. It is probable that progression of the asthma, with increase in the severity of the attacks, is due to persistence of the late phase reaction and a gradual increase in the mucosal inflammation. Lack of understanding of this, with consequent over-reliance on bronchodilators which overcome the acute attacks without modifying the underlying inflammation, could have contributed to the increase in asthma morbidity and mortality.


Extrinsic asthma and atopic asthma are two terms used interchangeably. It refers to the onset of wheezing, cough, shortness of breath upon contact of an allergen. The reaction is immunologic and mediated by IgE. 40% of the population has been reported to be atopic to an allergen, however only 5% of the population has asthma.


Cytokines is involvbed in atopic asthma.
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