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respiratory diseases

Asthma-Causes-Signs and Symptoms-Complications-Treatment

Asthma is a chronic inflammatory disorder of airways, that causes repeated episodes of breathlessness, chest tightness, cough and wheezing particularly at night or early in the morning. The airway obstruction which causes these symptoms are reversible.

Causes Of Asthma:
There are external and internal causes of asthma.
According to cause whether extrinsic or intrinsic asthma is divided into four types.

1. Extrinsic Asthma or atopic asthma:
       It is triggered by an immune response to some extrinsic stimuli, for example, dust particles, pollens and other irritants, it is characterized by an increased level of IgE antibodies

2. Intrinsic Asthma or non-atopic asthma:
      The immune reaction is not responsible for this type of asthma and Th 2 mediated immune response is not associated, rather it is triggered by non-immune stimuli such as pulmonary infections caused by viruses, cold, stress, exercise air pollutants e.g SO2 and NO etc. IgE levels are normal.

3. Drug-induced Asthma.
    The exact cause is unknown. Aspirin is very important in this case which causes drug-induced asthma. It is believed that aspirin inhibits Cyclooxygenase pathway of arachidonic acid metabolism without affecting the lipoxygenase pathway. which shifts the balance towards bronchospasm.

4. Occupational Asthma
      related to occupation, for example, mine workers, carpenters, industrial workers etc due to repeated exposure to the same antigen.


1. Genetic predisposition to type 1 hypersensitivity is the major cause,

2. The role of type 2 helper T cells is very important in asthma. Helper T cells secrete many substances among which, IL 4, IL 5 and IL 13 are important in the pathogenesis of asthma.
IL 4 Stimulates IG E production which is responsible for type 1 hypersensitivity.
IL 5 activates eosinophils
IL 13 causes hypersecretion of mucus.
all these factors predispose to asthmatic attack.

3. Airway remodelling is also involved in the pathogenesis of asthma. Although it requires a long time period to develop, it is important. Airway smooth muscles hypertrophy and increased deposition of collagen occur in the remodelling of airways in asthma. This result in bronchial hyper-responsiveness.

4. Recently a gene called ADAM33 is discovered that has some role in the pathogenesis of Asthma.

5. Mast cells secrete growth factors in asthma which cause smooth muscles hypertrophy and their mediators stimulate vagus nerve which causes reflex bronchospasm.

In asthmatic attack usually, two distinct phases occur (in case of atopic asthma)
1. Acute phase reaction.
    Acute phase reaction starts immediately after sensitized stimulus exposure, characterized by bronchoconstriction, wheezing, productive cough, and chest tightness etc. following mediators are involved in ACR
1. Leukotrienes C4, D4 and E4 cause, bronchoconstriction, Increase vascular permeability and increase mucin secretion.
2. Acetylcholine: released from pulmonary bronchial motor neurons causes bronchial smooth muscle contraction.
3. Histamine, causes increase bronchial constriction and Increase vascular permeability, but not much important because antihistamine drugs are not useful in treating asthma.
4. Prostaglandins D2, cause bronchoconstriction
5. Platelet-activating factor causes platelet aggregation and release of histamine

Late phase reaction.
Eosinophils and mediators released by them are responsible for the late phase reaction. Late phase reaction is an after effect of acute phase reaction starts 12 to 24 hours after the acute reaction. mediators released by eosinophils (for example Leukotriene C) causes bronchoconstriction. Eosinophil peroxidase damages tissue thus this amplify the inflammatory response even after the cessation of exposure to stimuli.

Clinical Signs and Symptoms:
Main signs and symptoms are.
1. Dyspnea (shortness of breath)
2. Weezing
3. Patient tries to inhale air but he can't exhale it, air trap in the lungs.
5. Symptoms last for 1 to several hours and relieve spontaneously or after therapy.
1. Hypercapnia (accumulation of Carbondioxide)
2. Acidosis
3. Respiratory failure

Bronchodilators: drugs that dilate bronchi e.g beta agonists (salmeterol, salbutamol, etc), and anticholinergics (e.g ipratropium)

Mast cell Inhibitors

Corticosteroids (reduce inflammatory response)

Leukotriene Inhibitors
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