About Asthma
Asthma is a chronic lung condition affecting
people all around the world. When an allergic reaction occurs in your chest, it
is called asthma.
Public
attention has recently focused on asthma because its prevalence and the
associated mortality rate have increased over the last several decades. While
familial aggregation is observed, no clear pattern of segregation can be
discerned. Multiple genetic, developmental, and environmental factors interact
to produce the overall condition.
Asthma
is a complex disease characterized by bronchial hyper-responsiveness (BHR),
inflammation, mucus production and intermittent airway obstruction. A person
with asthma may experience wheezing, shortness of breath, chest tightness, and
cough, particularly after exposure to an allergen, cold air, exercise, or
emotional stress. Asthma is treated with drugs; lifestyle changes can help
reduce exacerbations.
Signs
and Symptoms
The
main symptom of asthma is wheezing caused by obstruction of the airways. A
cough, sometimes with clear sputum, may also be present. The symptoms are very
variable, often with rapid onset, and associated with the triggers listed
above. Symptoms can be worse during the night or upon waking. Asthma sometimes
occurs with acid indigestion, especially amongst older patients.
Signs
of asthma are wheezing, rapid breathing, expiratory phase of breathing longer
than inspiratory, in-drawing of tissues between ribs and above sternum and
clavicles, over-inflation of the chest, and rhonchi (wheezy noises heard with a
stethoscope). During severe attacks the asthma sufferer may be cyanosed (blue),
may have chest pain and can lose consciousness. Between attacks a person with
asthma may show no signs at all.
Diagnosis
In most
cases the physician can make the diagnosis on the basis of typical symptoms and
signs. The typical rapid changes in airway obstruction can be demonstrated by
decrease in pulmonary function values at baseline, after exercise or inhalation
of histamine (less common) or methacholine (more common), and subsequent
improvement with an inhaled bronchodilator medication. Pulmonary function test
is required to make the diagnosis of asthma because many other lung diseases
can masquerade as asthma. Once the diagnosis is made, a peak flow meter can be
used to follow the disease.
Many
people with asthma have allergies; positive allergy tests support a diagnosis
of asthma and may help in identifying avoidable triggers. Some people with
asthma have been diagnosed with gastroesophageal reflux disease (GERD) and
immune related disorders including atopic dermatitis. Other tests (for example
chest X-ray or chest CT scan) may be required to exclude other lung disease
after pulmonary function testing has been obtained.
Pathology
Mechanisms
OK this
is going to be technical, so prepare yourself. Primary exposure to an antigen
or sensitization establishes the potential for asthmatic phenotypes. Following
entrapment of the antigen in the airway, the antigen is enzymatically degraded
by antigen presenting cells (APCs), such as dendritic cells. The peptide
becomes associated with a class II major histocompatiblity complex (MHC)
molecule. The complex moves to the surface of the APC where it is presented to
a T cell with a receptor specific for the MHC II peptide. Upon antigen
presentation and the appropriate costimulatory signal, T helper 0 (Th0) cells
become activated and begin to differentiate.
Under
the influence of interleukin (IL) 12, Th0 cells differentiate into T helper
type 1 (Th1) cells. IL4 induces Th0 cells to differentiate into T helper type 2
(Th2) cells. The differentiation of either type of T helper cell restricts the
differentiation of the other. Th1 cells primarily secrete IL2, interferon (IFN)
γ, and tumor necrosis factor (TNF) β. Th2 cells primarily secrete granulocyte
macrophage colony stimulating factor (GM-CSF), IL4, IL5, IL6, IL9, IL10, and
IL13. IL4 also enhances synthesis of IgE by antigen-stimulated B lymphocytes
that express surface receptors for the antigen. The antigen-specific antibodies
produced bind the FcεRI receptor on mast cells and dendritic cells in the
airway epithelium.
Subsequent
exposure of the same antigen to the cells of the airway epithelium initiates
the acute phase reaction. IgE-studded mast cells of the airway degranulate
causing release of vasoactive mediators such as histamine, increase the
synthesis of prostaglandins and leukotrienes, and increase the transcription of
cytokines. The mediators affect the bronchial mucosa by increasing mucosal
edema, mucus production, smooth muscle constriction, and chemotactic factors
which recruit other immune cells.
The
late phase is characterized by the influx of inflammatory and immune cells over
the next several hours after challenge. These cells, particularly eosinophils,
secrete a series of cytokines, leukotrienes, and polypeptides which contribute
to hyperresponsiveness, mucus secretion, bronchoconstriction, and sustained
inflammation.
This
process can cause the following:
- Infiltration of bronchial mucosa (the
lining of the airway) by lymphocytes
- Swelling (oedema) of bronchial mucosa
- Thickening of smooth muscle of
bronchioles
- Increased eosinophil granulocytes
- Mucus plugs
- Remodeling
(distortion) of the airway
Pathogenesis
- The fundamental problem seems to be
immunological: young children in the early stages of asthma show signs of
excessive inflammation in their airways.
- Epidemiology gives clues to the
pathogenesis: the incidence of asthma seems to be increasing worldwide;
asthma is more common in more affluent countries, and more common in
higher socioeconomic groups within countries.
- One theory is that it is a disease of
hygiene. In nature, babies are exposed to bacteria soon after birth,
"switching on" the Th1 lymphocyte cells of the immune system
which deal with bacterial infection. If this stimulus is insufficient (as,
perhaps, in modern clean environments) then asthma and other allergic
diseases may develop. This "Hygiene Hypothesis" may explain the
increase in asthma in affluent populations.
- Related to the above is another theory
regarding the part of our immune system which helps protect us against
parasites, such as tapeworms. The Th2 lymphocytes and eosinophil cells
which protect us against worms are the same cells responsible for the allergic
reaction. In the Western world these parasites are now rarely encountered
but the immune response remains and is triggered in some individuals by
certain allergens.
- A third theory blames the rise of
asthma on air pollution. While it is well known that substantial exposures
to certain industrial chemicals can cause acute episodes of asthma, it has
not been proven that the same is responsible for the development of asthma.
In
- Typical triggers include:
- inhaled allergens such as house dust
mite and cockroach, grass pollen, mold spores and pet epithelial cells.
- cold air
- exercise
- respiratory infection
- emotional stress
- aspirin & similar medications
Treatment
Options
Preventive
Triggers such as pets and aspirin
should be identified and managed. Current treatment protocols recommend an
inhaled corticosteroid (to suppress inflammation and reduce the swelling of the
lining of the airway) for anyone who has frequent or severe symptoms. If
symptoms persist, additional preventive drugs are added until the patient's
asthma is controlled.
- Inhaled corticosteroids (ex.
fluticasone, budesonide, beclomethasone, mometasone, flunisolide,
triamcinolone)
- Long-acting beta2-adrenoceptor
agonists (ex. salmeterol, formoterol, bambuterol, sustained-release oral
albuterol)
- Antimuscarinics/anticholinergics (ex.
ipratropium, oxitropium)
- Leukotriene modifiers (ex.
montelukast, zafirlukast, pranlukast, zileuton)
- Mast cell stabilizers (ex.
cromoglicate (cromolyn), nedocromil)
- Antihistamines are often used to treat
allergic symptoms which may underlie the chronic inflammation. In more
severe cases, hyposensitization ("allergy shots") may be
recommended.
- Omalizumab, an IgE blocker, can help
patients with severe allergic asthma that doesn't respond to other drugs.
However, it is phenomenally expensive and must be injected.
- If chronic acid indigestion (GERD)
contributes to a patient's asthma, it is necessary to treat it as well or
it will restart the inflammatory process.
Symptomatic
Episodes
of wheezing and shortness of breath generally respond to fast-acting bronchodilators.
Ordinarily these are provided in pocket-sized metered-dose inhalers, but for
patients with severe asthma a nebulizer is sometimes needed.
- Short-acting selective beta2-adrenoceptor
agonists (ex. albuterol (salbutamol), levalbuterol, terbutaline,
bitolterol, pirbuterol, procaterol, fenoterol, bitolterol, reproterol)
- Older, less selective adrenergic
agonists (ex. inhaled epinephrine and ephedrine tablets - both of which,
unlike other medications, are available over the counter in the
Advanced
When an
asthma attack is unresponsive to a patient's usual medication, other treatments
are available to the physician or hospital:
- Systemic steroids, oral or injected
(ex. prednisone, prednisolone, methylprednisolone, dexamethasone,
hydrocortisone)
- Oxygen to alleviate the hypoxia (but
not the asthma per se) that is the result of extreme asthma attacks
- Other bronchodilators that are
occasionally effective when the usual drugs fail:
- Non-specific beta-agonists, injected
or inhaled (epinephrine, isoetharine, isoproterenol, metaproterenol)
- Anticholinergics, IV or nebulized,
with systemic effects (glycopyrrolate, atropine)
- Methylxanthines (ex. theophylline,
aminophylline)
- Inhalation anesthetics that have a
bronchodilatory effect (isoflurane, halothane, enflurane)
- The dissociative anesthetic ketamine,
often used in endotracheal tube induction
- Magnesium sulfate, IV
- Intubation and mechanical ventilation,
for patients in or approaching respiratory arrest
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