Respiratory Medications PDF

Respiratory Medications Antihistamines, Decongestants, Antitussives, and Expectorants Are commonly used to manage symptoms of respiratory conditions like the common cold, allergies, and upper respiratory infections Antihistamines Mechanism of Action: Antihistamines block histamine receptors,...

Respiratory Medications Antihistamines, Decongestants, Antitussives, and Expectorants Are commonly used to manage symptoms of respiratory conditions like the common cold, allergies, and upper respiratory infections Antihistamines Mechanism of Action: Antihistamines block histamine receptors, specifically H1 receptors, to reduce allergic reactions. Histamine is a chemical released by the immune system during an allergic response, and it binds to H1 receptors in various tissues, such as the skin, respiratory tract, and blood vessels. By blocking histamine from binding to these receptors, antihistamines reduce symptoms such as sneezing, itching, nasal congestion, and runny nose. Common examples: Diphenhydramine (Benadryl), loratadine (Claritin), cetirizine (Zyrtec). Types: First-generation antihistamines (e.g., diphenhydramine) often cause sedation and drowsiness because they cross the blood-brain barrier. Second-generation antihistamines (e.g., loratadine, cetirizine) are less likely to cause sedation. Decongestants Mechanism of Action: Decongestants work by stimulating alpha-adrenergic receptors (α1 receptors) on the smooth muscles of blood vessels in the nasal passages. Activation of these receptors causes vasoconstriction (narrowing of the blood vessels), which reduces blood flow and thereby decreases the swelling of nasal tissues. This leads to relief of nasal congestion and improved airflow. Common examples: Pseudoephedrine (Sudafed), phenylephrine, oxymetazoline (Afrin). Important Considerations: Oral decongestants (e.g., pseudoephedrine) can cause systemic side effects like increased heart rate and blood pressure. Topical decongestants (e.g., nasal sprays like oxymetazoline) can cause rebound congestion if used for more than a few days, due to tolerance development. Antitussives (Cough Suppressants) Mechanism of Action: Antitussives work by suppressing the cough reflex. This is particularly useful for dry, non-productive coughs. Central-acting antitussives inhibit the cough center in the brain (medulla oblongata) to reduce the urge to cough.  Peripheral antitussives may act on the respiratory tract to reduce sensitivity and irritation. Common examples: Dextromethorphan (most common) is a central-acting antitussive that acts on the cough center in the brain to suppress coughing. Codeine is another central-acting antitussive that has opioid properties, which also suppresses coughing. Important Considerations: Dextromethorphan is a non-opioid antitussive and is often available over-the-counter. Codeine is an opioid and is generally used for more severe cases of coughing, with caution due to potential side effects and dependency risks. Expectorants Mechanism of Action: Expectorants work by increasing the production of mucus and reducing the viscosity of the mucus in the airways. This helps to clear mucus from the respiratory tract, making it easier to cough up and clear the airways. The primary mechanism involves increasing hydration in the respiratory secretions and reducing the stickiness or thickness of mucus. Common example: Guaifenesin (Mucinex). Important Considerations: Guaifenesin is typically considered safe and is often included in combination with other cold medications. It is essential to stay well-hydrated while taking expectorants to enhance their effectiveness. Respiratory Drugs Respiratory drugs are used to treat a variety of respiratory conditions, including asthma, chronic obstructive pulmonary disease (COPD), allergies, and upper respiratory infections. These medications work through different mechanisms to relieve symptoms, improve lung function, and reduce inflammation. Bronchodilators Bronchodilators relax the muscles around the airways to allow the airways to open up, making breathing easier. They are commonly used to treat conditions like asthma and COPD. Beta-2 Adrenergic Agonists Mechanism of Action: These drugs stimulate beta-2 adrenergic receptors in the smooth muscles of the bronchi (airways) in the lungs. Activation of these receptors leads to smooth muscle relaxation and bronchodilation, which helps to open up the airways. They are fast-acting and are often used in emergencies (e.g., during an asthma attack). Common Examples: Short-acting beta-agonists (SABA): Albuterol (Salbutamol), Levalbuterol. Long-acting beta-agonists (LABA): Salmeterol, Formoterol. Anticholinergics (Muscarinic Antagonists). Mechanism of Action: These drugs block muscarinic receptors (M1, M2, M3) in the smooth muscle of the lungs, which are normally activated by acetylcholine (a neurotransmitter released by the parasympathetic nervous system). By blocking these receptors, anticholinergics prevent bronchoconstriction. They are particularly useful in COPD and can be used alongside beta-agonists. Common Examples: Short-acting muscarinic antagonists (SAMA): Ipratropium. Long-acting muscarinic antagonists (LAMA): Tiotropium, Aclidinium. Corticosteroids Corticosteroids reduce inflammation in the airways and are used to manage chronic inflammation in conditions like asthma and COPD. Inhaled Corticosteroids (ICS) Mechanism of Action: Inhaled corticosteroids (e.g., fluticasone, budesonide) work by reducing inflammation in the airways, suppressing the immune response, and decreasing mucus production. They inhibit the release of inflammatory mediators (such as cytokines, leukotrienes, and prostaglandins) and reduce the infiltration of inflammatory cells (e.g., eosinophils, T-cells). They are typically used for long-term management of asthma and COPD. Oral/Systemic Corticosteroids Mechanism of Action: These are used for short-term flare-ups or in severe cases. They have the same mechanism as inhaled corticosteroids but are taken systemically, resulting in broader effects and more potential side effects (e.g., weight gain, osteoporosis). Common Examples: Inhaled corticosteroids: Fluticasone, Budesonide, Beclometasone. Systemic corticosteroids: Prednisone, Methylprednisolone. Leukotriene Modifiers Leukotrienes are inflammatory mediators involved in asthma and allergic reactions. Leukotriene modifiers are used to prevent bronchoconstriction, inflammation, and mucus production. Leukotriene Receptor Antagonists (LTRAs) Mechanism of Action: These drugs block leukotriene receptors (specifically CysLT1 receptors) on bronchial smooth muscle cells and other cells involved in inflammation. By blocking leukotrienes (especially leukotriene D4), they prevent bronchoconstriction and airway inflammation. Common Example: Montelukast (Singulair), Zafirlukast (Accolate). 5-Lipoxygenase Inhibitors Mechanism of Action: These drugs block 5-lipoxygenase, the enzyme responsible for the formation of leukotrienes from arachidonic acid. By inhibiting this enzyme, they prevent the synthesis of leukotrienes, which reduces inflammation and bronchoconstriction. Common Example: Zileuton (Zyflo). Mast Cell Stabilizers Mast cell stabilizers are used to prevent the release of histamine and other inflammatory mediators from mast cells, which are involved in allergic reactions. Mechanism of Action: These drugs prevent the release of histamine, leukotrienes, and other mediators from mast cells when they are exposed to allergens or irritants. This helps reduce inflammation and bronchoconstriction. Common Examples: Cromolyn Sodium (Intal), Nedocromil (Tilade). Phosphodiesterase-4 (PDE4) Inhibitors These are used primarily in the management of severe COPD. Mechanism of Action: PDE4 inhibitors block the enzyme phosphodiesterase-4, which normally breaks down cyclic AMP (cAMP) in cells. By inhibiting PDE4, these drugs increase cAMP levels in inflammatory cells, leading to reduced inflammation, bronchoconstriction, and mucus production. Common Example: Roflumilast (Daliresp). Immunomodulators (Biologics) Biologics are newer treatments for severe asthma, especially in patients with allergic or eosinophilic asthma. They target specific immune system components. Monoclonal Antibodies Mechanism of Action: These drugs target specific cytokines or immune cells involved in inflammation: ○ Anti-IgE (Omalizumab): Binds to IgE, preventing it from interacting with mast cells and basophils, thus reducing allergic reactions. ○ Anti-IL-5 (Mepolizumab, Reslizumab): Block the action of interleukin-5 (IL-5), which is involved in the maturation and activation of eosinophils, a type of white blood cell that plays a role in inflammation in asthma. ○ Anti-IL-4/IL-13 (Dupilumab): Block interleukins 4 and 13, which are important in the inflammatory response in asthma. Common Examples: Omalizumab (Xolair), Mepolizumab (Nucala), Dupilumab (Dupixent). Cough Suppressants (Antitussives) Antitussives reduce coughing by acting on the cough reflex in the brain. Mechanism of Action: Central-acting antitussives (e.g., dextromethorphan) suppress the cough center in the medulla of the brain, reducing the urge to cough.  Peripheral antitussives (e.g., menthol or camphor) reduce irritation in the airways, though these are less commonly used in modern clinical practice. Common Examples: Dextromethorphan, Codeine. Expectorants Expectorants help clear mucus from the airways. Mechanism of Action: Expectorants (e.g., guaifenesin) work by increasing the production of thinner mucus, making it easier to clear mucus from the airways and reduce coughing. They may also help in loosening up thick mucus in the lungs, facilitating its expulsion. Common Example: Guaifenesin (Mucinex).