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Diagnosis of Asthma & Prevention and Treatment Drugs For Asthma

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Diagnosis of Asthma

Exacerbations of asthma symptoms equates to an individual’s control of their asthma. To prevent long term complications of airway remodeling, early detection with an accurate diagnosis is needed to exclude other diseases and causes for difficulty breathing. For example, Chronic obstructive pulmonary disease, Congestive heart failure, Pulmonary embolisms or mechanical obstruction (from tumors). Asthma diagnosis is based on several factors, including a detailed medical history, a physical exam, symptoms and overall health and test results.

 

Prevention For Asthma 

 

Prevention of exposure to known triggers is warranted. Hyposensitization may be beneficial if the asthma has an allergic mechanism, in such cases:

      •  Identify and avoid asthma triggers.
      •  Identify and treat attacks early and monitor breathing.
      •  Other measures include dust free house.
      •  Intake of selective type of food.
      •  Avoid exposure to extreme cold condition.
      •  Get vaccinated for influenza and pneumonia..

Treatment for Asthma

 

Pharmacological Treatment: Drug therapy depends on frequency and severity of attacks. The bronchodilators are often considered rescue inhalers, while the other medications are considered more prophylactic or therapeutic medications.
  1. Bronchodilators (Sympathomimetics): The mechanism of action for sympathomimetic bronchodilators is to bind the receptors in airway smooth muscle thus causing bronchodilation and increased ciliary beat frequency. e.g. Albuterol, Salbutamol and Terbutaline.
  2. Anticholinergic agents: The effect of anticholinergic bronchodilators are bronchodilation through inhibition of bronchoconstriction secondary to blockade of the effects of acetylcholine. The mechanism of action for anticholinergic bronchodilators is non-selective antagonism of muscarinic receptors leads to down regulation of cGMP which results in bronchodilation. Additional acetylcholine is released in response, thus overcoming the effect in smooth muscle. e.g. Ipratropium, Aclidinium.
  3. Corticosteroids: The effect of inhaled corticosteroids is reduced airway inflammation. Overall airway bronchial hyper-responsiveness decreases. Improved asthma control and increased sensitivity of β-receptors in smooth muscle. The mechanism of action for inhaled corticosteroids is to suppress granuloma formation, reduce arachidonic acid metabolism, up-regulate β-adrenergic receptors on leukocytes, and decrease synthesis of prostaglandins and leukotrienes. e.g. Beclomethasone, Flunisolide, Triamcinolone.
  4. Biologic Response Modifiers (Monoclonal Antibodies): The effect of Biologic Response Modifiers is decreased frequency of allergen induced asthma exacerbations. The mechanism of action for Biologic Response Modifiers is, when the monoclonal antibody binds to IgE, interfers with mast cell binding. This prevents mast cell degranulation and release of inflammatory mediators. Cytokine release seen in the late phase of an allergic reaction is also prevented through blocking the receptors on dendritic cells, epithelial cells, eosinophils, monocytes and platelets. E.g. Omalizumab.
  5. Leukotriene Receptor Antagonists: The effect of leukotriene receptor antagonists is prevention of allergen induced bronchoconstriction. The mechanism of action for leukotriene receptor antagonists is antagonism of cysteinyl-leukotriene receptors, thus preventing histamine release. e.g. Montelukast and Zafirlukast.
  6. Mast Cell Stabilizers: The effect of mast cell stabilizers is prevention of bronchocon-striction and inflammation. The mechanism of action of mast cell stabilizers is to antagonize mast cell degranulation to prevent the release of histamine and other mediators of allergic reaction. Agents do not interfere with IgE. The anti-inflammatory mechanism is unknown. e.g. Cromolyn and Nedocromil
  7. Methylxanthene Derivatives: The mechanism of action for methylxanthene derivatives is bronchodilation. The mechanisms of action include prostaglandin antagonism, stimulation of endogenous catecholamines, inhibition of calcium influx into smooth muscle (preventing muscle contraction), antagonism of adenosine receptors, and inhibition of release of mediators from leukocytes and mast cells. E.g. Theophylline.
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