Asthma is an autoimmune disorder in which external or internal events, such as airborne allergens, foods, temperature extremes and exercise, trigger unnecessary inflammation of the bronchial tubes. Symptoms of asthma include shortness of breath, frequent coughing, pain, pressure, or tightness in the chest, and wheezing. The inflammatory process creates this typical cluster of symptoms in spite of heterogeneous factors, including biochemical, cellular, and molecular variations, that control its expression and severity. As a result, the underlying disease process can vary widely from one individual to another even though the symptoms may be similar (Jarjour et al., 2012). Underlying processes include bronchospasm (bronchial tube constriction), increase in mucus production, and swelling of the bronchial tube walls.Prescription/nonprescription meds, categories, mechanism of action and desired outcomes

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Both prescription and nonprescription medications are available for the treatment of asthma. Epinephrine and ephedrine are nonprescription drugs that reduce bronchospasm; however, they are not effective against other inflammatory symptoms such as swelling from fluid in the walls of the bronchial tubes (Agarwal et al., 2016). Their action is based on stimulation of beta receptors in the sympathetic nervous system. Therefore, they have many potentially adverse effects such increased heart rate and blood pressure.

Prescription asthma medications fall into several categories: bronchodilators, corticosteroids, leukotriene modifiers, and mast cell stabilizers (Bateman et al., 2015). Bronchodilators relax the muscles of the bronchial tubes, widening the air passages. There are three classes of bronchodilators. Beta2-adrenoreceptor agonists (e.g. albuterol) act by relaxing the smooth muscle that lines the bronchial tubes (the nonprescription bronchodilators are also in this class). Beta agonists can be short-acting or long-acting. Short-acting inhaled beta agonists are sometimes called “rescue inhalers” because they are designed to stop an asthma attack that has already begun, whereas long-acting beta agonists and other drugs have a desired outcome of attack prevention. Anticholinergic bronchodilators (e.g. tiotropium) antagonize the muscarinic receptors, preventing the parasympathetic nervous system from constricting the airways. Methylxanthines (e.g. theophylline) dilate the airways by inhibiting phosphodiesterase, thereby increasing cyclic AMP in the cells (Agarwal et al., 2016).

Dexamethasone and prednisone are examples of corticosteroids that may be used in the treatment of asthma. They function by inhibiting immune responses and inflammation. Leukotriene modifiers reduce the action of leukotrienes, which are secreted by mast cells, basophils and eosinophils. Leukotrienes increase mucus production and produce constriction and swelling in the lungs. Leukotriene receptor antagonists keep leukotriene from bonding with its receptor, while leukotriene synthesis inhibitors interfere with an enzyme, 5-lipoxygenase, which is required for synthesis of leukotrienes. Finally, mast cell stabilizers are a kind of calcium channel blocker which prevents sensitized mast cells from releasing inflammatory chemicals (Bateman et al., 2015).

Since asthma is a progressive disease, it is essential for the patient to be closely monitored both for progression of asthma symptoms and for adverse effects of asthma treatments. Most drugs used to treat asthma can have adverse effects, including life-threatening anaphylaxis (Agarwal et al., 2016). Some asthma medications, if taken during pregnancy, can cause congenital malformations (Nelson et al., 2012). Also, they can have moderate to severe interactions with other drugs. For example, albuterol can cause shakiness of extremities, trembling, palpitations, cough, and sympathetic nervous system activation. Its primary interaction is the antagonism of beta-blockers, which are often used in the treatment of hypertension and heart disease. Albuterol and other bronchodilators can also interact with nadolol, fingolimod, mifepristone, and a large number of other drugs (Bateman et al., 2015). Long acting beta agonists have been found to increase deaths from asthma and to cause more serious asthma exacerbations, or sudden worsening (NHLBI, 2012). Therefore, these drugs carry an FDA “black box” warning.

Corticosteroids increase the chances of infections, pancreatitis, GI bleeding, mental status changes, and hypertensive crisis. They interact with hydrocodone, live vaccines, ticagrelor, ciprofloxacin, etanercept, mifepristone, sonidegib, vigabatrin, and many other drugs. However, the interactions generally are not as serious as those caused by bronchodilators (Agarwal et al., 2016). Leukotriene modifiers may produce abdominal pain, flu-like symptoms, headache, joint pain, pus in the urine, and mental status changes. They interact with drugs such as barbiturates, carbamazepine, sulfa drugs, divalproex, rifampin, and vilazodone. Finally, cromolyn, which is an example of a mast cell stabilizer, may cause hives, itching, low blood pressure, chest tightness, cough, nausea, and unpleasant taste (Bateman et al., 2015). Cromolyn is known to interact with inhaled insulin.

Approximately thirty percent of patients do not respond to inhaled corticosteroids, which are the cornerstone of step therapy in treatment of asthma. Researchers continue to investigate new drugs, such as ultra long-acting beta agonists, interleukin pathway modulators, toll-like receptor 9 agonists, and tyrosine kinase inhibitors. The expectation is that these drugs will improve asthma prevention, thereby reducing disease progression and airway remodeling (Olin & Wechsler, 2014).

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