Bronchial Asthma definition , causes , triggers and pathogenesis

Here we are going to discuss Bronchial Asthma regarding its definition , aetiology ( causes ) and pathogenesis , and will continue to diagnosis and management soon in another post .

What is  Bronchial asthma ?

 Bronchial asthma is an inflammatory disease of airways that is characterized by increased responsiveness of the tracheobronchial tree to a multiplicity of stimuli.
bronchial asthmaIt is pathologically characterized by a widespread narrowing of the air passages and clinically by paroxysmal attacks of dyspnea and wheezy chest which may be relieved spontaneously or as a result of therapy.

What are the causes of Bronchial Asthma ?

Causes and types:
 Etiologic or pathologic classification of the disease is difficult, however, asthma traditionally is divided into two forms.

a. Extrinsic asthma : ( Atopic or Allergic )

(usually there is a definite external cause, mostly atopic)
Characterized by:

1- Early childhood (early onset asthma)
2- It occurs mostly in atopic individuals and usually with + ve. Family History of atopy e.g urticaria or allergic rhinitis. It is usually seasonal !?
3- IgE increases , so it is a classic type 1 IgE mediated hypersensitivity reaction to an inhaled antigen i.e (Immunologically mediated).

Antigen + IgE --> mast cell ---> release of mediators --->  bronchospasm

4- It is usually triggered by antigenic stimuli (allergens) .
5- Prognosis :  good due to Natural desensitization

Examples of antigens
1- Pollens, animal dander                                         2- Dust, Mites
3- Drugs e.g. penicillins, cephalosporines, sulfa         4- Food allergy.

b. Intrinsic: or cryptogenic Asthma

 (non atopic, the primary cause of increased airway reactivity is unkown !?)
Characterized by:
1- Starts in middle age (late onset) .
2- -ve family history (for atopy)
3- No evidence of immediate hypersensitivity to specific Ag.
4- Ig A  increases  in some cases .
5- It is usually triggered by respiratory tract infections, chemicals or drugs.

Pathogenesis of bronchial asthma 

(The inflmmatory process and its biochemical mediators)

1- Atopic (allergic or extrinsic asthma):

It is triggered by environmental antigens (dust, pollens, food ...) often with a positive F.H of atopy.
 It is a classic type 1 IgE mediated hypersensitivity reaction having :

• Acute phase with binding of Antigen (Ag)  by IgE coated mast cells causing release of primary mediators (histamine, eosinophil and neutrophil chemotactic factors) and secondary mediators (Ieukotrienes, P.G, cytokines e.g IL4, IL5) these acute mediators result in bronchospasm, edema, mucus seccetion and recruitment of leukocytes .

• A late phase reaction (cellular phase) is mediated by recruited leukocytes (eosinophils, basophils, neutrophils) causing bronchospasm and edema with
leukocytic infiltration .

2- Non atopic (non allergic or intrinsic asthma):

The mechanism of bronchial inflammation and hyperresponsiveness is much less clear in patients with intrinsic asthma.
It is often triggered by viral respiratory tract infections, chemical irritants and drugs with no evidence of IgE mediated hypersensitivity.
The primary cause of increased airway reactivity is unknown.
 Some mediators e.g serotonin , prostaglandins (PG)  and thromboxanes cause tissue inflammation and may particularly
important in the pathogenesis of this type of asthma. 

** Triggers of asthma or precipitating factors:

1- The above antigens (1, 2, 3,4). 
2- Aspirin sensitive. Aspirin inhibits P.G synthesis ----> +++  production of Ieukotrienes from arachidonic acid, this is common in patients with allergic rhinitis with nasal polyps . (this also occur with other NSAID).
3- Exercise induced asthma due to thermal changes within bronchial tree (Cooling and drying of bronchial mucosa) .
4- Occupational asthma e.g. Byssinosis, spray painting, bakers, wood dust, varnishes and metal salt (Nickel).
5- Allergic bronchopulmonary aspergillosis 
7. Aspergillus Ab in the serum of some patients.
6- Viral infection of respiratory tract e.g respiratory syncytial virus, rhinovirus or parainfluenza virus.
7- Stress induced asthma. 
8- Cold air or dry air.
The tracheobronchial tree of asthmatic individuals appears to have an exaggerated reactivity (non specific bronchial hyperreactivity), to distinguish it from the
bronchospasm provoked by immunologically specific antigens. The mechanisms underlying bronchial hyperreactivity are:

(1) Muscle reactivity i.e a change in the contractile mechanisms of airway smooth muscle.
(2) Autonomic reactivity:
             (a) Parasympathetic system appears to mediate the reflex bronchial constriction.
             (b) A deficiency in the sympathetic nervous system may be responsible for bronchial hyperactivity.
             (c) The non adrenergic inhibitor system, it seems to inhibit bronchial constriction, deficiency of this system ---> bronchospasm.
(3) Invironmental factors e.g respiratory viral infections.

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