"Bronchial asthma is characterised by episodic acute limitation of airflow,
reversing either spontaneously or in response to treatment."
When discussing possible causes of asthma is important to distinguish what is meant by 'cause'. Many people believe that the increase in asthma seen over the past few decades in the United Kingdom is due to increased pollution. Unfortunately the available data do not support this theory - pollution levels in the UK have actually fallen steadily over the last 40 years! The pollution may on bad days affect asthma sufferers more than the general population but there is little to suggest that pollution actually causes an increase in the number of people who are asthmatic
A distinction is needed to describe agents that actually cause asthma from those that merely make pre-existing asthma periodically worse. Agents that can actually cause asthma are known as sensitising agents. Agents that might trigger an asthma attack in an asthmatic subject are called triggering agents.
It should be noted that sensitising agents will not necessarily cause asthma in everyone. Not everyone who is exposed to house dust mites develops asthma. It seems that some people are more susceptible to such agents than others. Why is not fully known. Various theories abound but it is at least in part a result of genetic predisposition.
Triggers elicit asthmatic attacks in asthmatic subjects by irritating the already inflamed and hyperreactive airways. Indeed triggers such as cold air or methacholine (a signalling chemical naturally present in the body) are used by doctors to measure the degree of reactivity of patients lungs. Characteristically, the lungs of asthmatic subjects react to far lower amounts of trigger than the lungs of healthy control subjects.
Asthma is now most commonly described amongst experts as an inflammatory response disease. It has been suggested that the two main causes of breathlessness - airway wall inflammation and airway wall constriction - are both due to the release inflammatory response chemical signals.
To understand the pathophysiology of asthma a little backround airway anatomy is required. We breath through our noses and mouths. To reach the lungs both these inlets converge on the trachea (the windpipe) below which an upside down tree like structure occurs. Two main branches (bronchi) split, one to each lung. Gradually more and branches and twigs (the bronchioles) split off to eventually end in the alveoli. Like the leaves of a tree, the alveoli are effectively cul-de-sacs. It is in the alveoli that fresh oxygenated air enters the bloodstream and stale (carbon dioxide-loaded) air comes out again.
Asthma effects only the bronchi and bronchioles, not the alveoli. The bronchi and bronchioles are tubes through which air must pass to reach the alveoli, and thus be absorbed into the blood. In asthma these tubes become partly or completely blocked. This results in difficulty or impossibility to breath.
The airway tubes are lined with a layer of cells known a the epithelial layer. Normally this layer is involved in 'brushing' mucous up the airways by means of hair-like cilia. The cilia act like a conveyor sending the mucous up the airways until finally it can be swallowed. This mucous conveyor carries any foreign particles out of the lung. When it stops or is damaged mucous can build up and block the lungs.
The epithelial layer of cells in asthmatic subjects is often inflamed and damaged. A damaged or scarred epithelial layer can allow foreign particles to penetrate the lung lining more easily. In response to foreign particles the cells release signalling chemicals which can make the damage worse.
Sensitising agents (or allergen as they are sometimes called) are specific. Where asthma is due to an allergy, the resulting response to the specific allergen is far, far greater in the asthmatic subject than the normal subject. In other words, tiny amounts of allergen can cause an asthmatic response.
Allergens act by being inappropriately recognised by the body's defensive immune system. Special chemicals called antibodies recognise the allergen and initialise a cellular response. Cells release signalling chemicals which 'warn' other cells with the result that they to release signalling chemicals. These chemicals produce a number of effects. One such chemical, histamine, can cause the muscle encircling the airways to contract, thereby narrowing the diameter of the airways.
The level of antibodies throughout the body is normally tightly controlled. The levels rise during infections as antibodies seek out bacteria or viruses so that special killer cells can deal with them. In asthmatic subjects there is often an increase in the levels of certain antibodies even in the absence of infection.
Since the epithelial layers that line the lung are often damaged in asthmatics, foreign particles can more readily penetrate the lung lining. This, coupled with the increased numbers of antibodies, results in an immune allergic response. When antibodies find a specific foreign particle, the antibodies signal to special cells known as mast cells. Mast cells in turn release more signalling chemicals. The resulting signal cascade sparks of an asthmatic response, firstly by causing the airway smooth muscle to contract and secondly to produce further inflammation and damage.
There is a large number of treatments available for asthma. Whilst environmental (and therefore allergen) control measures are often to be encouraged, there remains a need to treat the underlying inflammation characteristic of an asthmatic's airways. Pharmacological intervention in asthma is either preventative or curative. The former tends to target the underlying chronic inflammation of the airway walls in a bid to reduce the hyperreactivity. The latter approach to treatment is used in the acute phase of the disease in which an asthmatic attack is actually present. Some common classes of drug for asthma treatment are listed below. The information for each drug type gets more detailed as the definition progresses so just read up to where you feel comfortable!