Drugs and the Respiratory System PDF

DRUGS AND THE RESPIRATORY SYSTEM Bronchodilators TERMINOLOGY  ASTHMA a respiratory disease characterized by bronchoconstriction, shortness of breath (dyspnea) and wheezing. EMPHYSEMA a p...

DRUGS AND THE RESPIRATORY SYSTEM Bronchodilators TERMINOLOGY  ASTHMA a respiratory disease characterized by bronchoconstriction, shortness of breath (dyspnea) and wheezing. EMPHYSEMA a progressive lung disease that is part of Chronic Obstructive Pulmonary COPD Disease (COPD), causes destruction of the walls of the alveolar sacs. leading chronic obstructive pulmonary disease; to reduced surface area for gas usually characterized by emphysema exchange and difficulty breathing and chronic bronchitis CHEMICAL MEDIATOR CHRONIC BRONCHITIS substance formed by mast cells, certain respiratory condition caused by chronic blood cells, and other body cells and irritation that increases secretion of that is released during inflammatory mucus and causes degeneration of the and allergic reactions respiratory lining.  PROSTAGLANDINS SRS-A slow-reacting substance of anaphylaxis; series of chemical mediators that are a prostaglandin derivative that is a released by most body cells and are potent bronchoconstrictor and often involved in disease processes mediator of asthma. HISTAMINE LEUKOTRIENES substance that interacts with tissues to substance formed from arachidonic acid produce most of the symptoms of which participates in inflammatory allergy reactions (prostaglandins). May act as a slow-reacting substance in anaphylaxis. ECF-A eosinophilic chemotactic factor of anaphylaxis; released by mast cells and BRONCHOCONTRICTION functions to attract eosinophils to the narrowing of the airways sire of cell injury and irritation.  MUCOLYTICS BRONCHODILATORS Drugs that liquefy/thin ouy bronchial drugs that relax bronchial smooth mucus muscle and dilate the lower respiratory passages to allow better airflow CORTICOSTEROIDS synthetic substances used in treating XANTHINES inflammatory and allergic diseases a purine compound found in most bodily tissues and fluids; it is a precursor of uric acid. Methylated EXPECTORANTS xanthine compounds such as caffeine agents which stimulate the production and theophylline are used for their of respiratory secretions, which then bronchodilator effects. decrease the irritation and cough caused by excessive dryness of the airways  ASTHMA 2 May also include mucosal 1 An inflammatory condition of the respiratory system edema, increased characterized by shortness production of bronchial of breath and wheezing mucus, and depression of caused by bronchiolar ciliary activity in constriction respiratory tract 3 In susceptible patients, asthma attacks can be caused by: Irritants (dust, pollutants, noxious chemicals) Exercise (particularly in cold weather) Respiratory tract infections Aspirin and related drugs (NSAIDs) Allergy to foreign proteins (pollen and animal dander)  CILIARY DEPRESSION VS MUCUS PRODUCTION CILIARY DEPRESSION Definition: Refers to the reduced function or impairment of the cilia, the tiny hair-like structures lining the respiratory tract (mainly the bronchi and bronchioles). Role of Cilia: Cilia are responsible for moving mucus along the airways toward the throat, where it can be swallowed or expelled. Helps to remove particles, dust, pathogens, and excess mucus from the lungs. Effect of Depression: When suppressed or impaired, mucus cannot be cleared effectively, which can lead to mucus buildup, airway obstruction, and increased risk of respiratory infections. Can be caused by inflammation, exposure to irritants (e.g., cigarette smoke), infections, or certain medications. MUCUS PRODUCTION Definition: Refers to the secretion of mucus by the respiratory tract. Mucus is essential for trapping foreign particles, pathogens, and debris, helping protect the lungs from infection and irritation. In Asthma: In people with asthma, inflammation leads to hypersecretion of mucus, meaning that more mucus is produced than normal. This is a common feature during asthma exacerbations, where excess mucus can block the airways, making breathing difficult. Mucus Hyperproduction: Conditions like asthma, chronic bronchitis, and other respiratory diseases often involve excess mucus production. This thick, sticky mucus can be difficult to clear, especially when ciliary function is impaired. THE ROLE OF CHEMICAL MEDIATORS IN ASTHMA 1 During an inflammatory reaction chemical mediators are formed and released from injured tissue, mast calls, and leukocytes in the respiratory tract 2 They are responsible for symptoms and complications of asthma Mediators include Histamine, ECF-A, and SRS-A 3 Histamine in respiratory tract causes bronchoconstriction, mucosal edema, and infiltration of eosinophils 4 ECF-A (eosinophilic chemotactic factor of anaphylaxis) is released by mast cells to attract eosinophils to site of cell injury or irritation, they are part of the general inflammatory reaction THE ROLE OF CHEMICAL MEDIATORS IN ASTHMA 4 Prostaglandins are widely distributed in many body tissues and are released by cell membranes in response to injury or irritation, which causes swelling 5 Specifically in lungs and with asthma, the prostaglandin complex SRS-A (Slow Reacting Substance of Anaphylaxis) is released, made up of three leukotrienes (type of prostaglandin) 6 SRS-A is a potent bronchoconstrictor with long duration, promotes mucosal edema, secretion of mucous, leukocyte infiltration These mediators are responsible for the characteristic airway hyperresponsiveness, mucus hypersecretion, and chronic inflammation observed in asthma  HISTAMINE 140 120 Source: Released from mast cells during allergic 100 reactions. 80 Effects: In the respiratory tract, histamine causes: Bronchoconstriction: Narrowing of the airways, 60 making it difficult to breathe. Mucosal edema: Swelling of the airway lining, 40 further narrowing the airways. Infiltration of eosinophils: Recruitment of 20 eosinophils (a type of white blood cell) to the airways, which contributes to inflammation and 0 Item 1 Item 2 Item 3 Item 4 Item 5 tissue damage. Outcome: Histamine’s action leads to immediate allergic responses and contributes to acute asthma symptoms like shortness of breath and chest tightness.  ECF-A (Eosinophilic Chemotactic Factor of Anaphylaxis) 140 Source: Released by mast cells during an allergic or 120 inflammatory reaction. 100 Effects: 80 ECF-A attracts eosinophils to the site of injury or irritation in the respiratory tract. 60 Eosinophils are involved in the late-phase allergic response and contribute to the chronic 40 inflammation seen in asthma. They release toxic proteins and enzymes that can damage 20 the airway tissues, leading to ongoing inflammation and hyperresponsiveness. 0 Item 1 Item 2 Item 3 Item 4 Item 5 Outcome: ECF-A and the recruited eosinophils help sustain the inflammatory reaction, making asthma a chronic, ongoing condition rather than a one-time acute event.  SRS-A (Slow-Reacting Substance of Anaphylaxis) 140 Composition: This term refers to leukotrienes (mainly LTC4, 120 LTD4, and LTE4), which are potent bronchoconstrictors. 100 Source: Released from mast cells and other immune cells (like basophils). 80 Effects: 60 Prolonged Bronchoconstriction: Leukotrienes cause 40 long-lasting narrowing of the airways. Increased Vascular Permeability: They promote swelling 20 of the airway lining by increasing the leakiness of blood vessels. 0 Excess Mucus Secretion: Leukotrienes stimulate excess Item 1 Item 2 Item 3 Item 4 Item 5 mucus production, which can block the airways. Outcome: SRS-A contributes to sustained airway obstruction in asthma, making it harder to breathe and exacerbating asthma attacks.  ASTHMA THERAPY Goals: Therefore…want to stop or slow down Maintain normal these chemical mediators to treat activity levels symptoms of asthma Prevent symptoms( i.e cough, wheezing, dyspnea) Classes of drugs most commonly Maintain normal used: spirometry Prevent exacerbations Bronchodilators Avoid side effects of Corticosteroids therapy Anti-allergics Leukotriene receptor antagonists  COPD Chronic Obsructive Pulmonary Disease Chronic Obstructive Pulmonary Disease Progressive respiratory condition caused by emphysema and chronic bronchitis. Both conditions cause irreversible changes to the respiratory system. Symptoms include: chronic cough SOB increased susceptibility to infection restriction of physical activity.  Chronic Cigarette smoking and other 01. environmental pollutants increase Bronchitis secretions and thicken mucus which interferes with gas exchange (when severe may cause cyanosis) “Blue Bloaters” Secretions over time cause 02. Chronic irritation and inflammation of the fibrotic changes (degeneration of respiratory tract respiratory cells) in the respiratory lining Mucus obstructing airways = Bronchitis = Boogers Treatment usually palliative, 03. Lack of O2, increase CO2 = cyanosis help them breath, but cannot (bluish discolouration of skin) reverse the changes in the fibrotic lining  “Pink Puffers” used to describe patients with emphysema, another form of COPD. They tend to be Irreversible lung damage thinner, have a "puffed" appearance due to forces patients to increased respiratory effort, and do not decrease daily activities typically exhibit cyanosis because they can maintain better oxygenation despite their breathing difficulties. Those with emphysema are exhausted since they Emphysema Permanent enlargement of expend 15-20% of total alveoli and destruction of energy just to breathe alveolar walls caused by smoking and hereditary factors Treatment includes respiratory exercises, O2 therapy, and medications Lungs lose their (bronchodilators and elasticity making the mucolytics) expiration of air very difficult  COPD Therapy Goals: Drug therapy provides some relief but not able to reverse physical damage to the respiratory lining Decrease or abolish dyspnea (SOB) Reduce impairment, disability & physical limitations Reduce frequency & severity of exacerbations Improve quality of life Palliative at end stages  RESPIRATORY CONDITIONS COMPARISON CHRONIC ASTHMA COPD BRONCHITIS A progressive disease that encompasses two a type of chronic obstructive pulmonary disease A chronic inflammatory disorder of the airways main conditions: chronic bronchitis and characterized by reversible airway obstruction. (COPD) leading to excessive mucus production emphysema. It is characterized by persistent and persistent cough. airflow limitation Often triggered by allergens (pollen, dust mites, pet dander), irritants (smoke, strong odors), Causes: Primarily caused by long-term Primarily caused by smoking, but can also be exposure to irritants, particularly cigarette exercise, cold air, and respiratory infections. influenced by long-term exposure to pollutants, smoke, but also air pollution and occupational dust exposures. Symptoms: Wheezing, coughing (especially at night or early morning), shortness of breath, Symptoms include chronic cough, excessive and chest tightness Symptoms: A persistent cough that produces sputum production, shortness of breath mucus (often called "smoker's cough"), (especially during exertion), and fatigue. shortness of breath, and frequent respiratory Involves airway hyperresponsiveness, Symptoms tend to worsen over time. inflammation, and increased mucus infections. production. COPD involves both airway inflammation and Involves inflammation of the airways, mucus destruction of lung tissue (as seen in gland hyperplasia, and narrowing of the air The airway obstruction is typically reversible emphysema), leading to irreversible airway with bronchodilators. passages. Unlike asthma, the airway obstruction and impaired gas exchange. obstruction in chronic bronchitis is usually not Management: Controller medications (inhaled fully reversible. Treatment includes: smoking cessation, corticosteroids, leukotriene modifiers) and bronchodilators, corticosteroids, oxygen quick-relief inhalers (short-acting beta- Treatment focuses on smoking cessation, therapy (if needed), and pulmonary bronchodilators, corticosteroids, and pulmonary agonists) are used to manage symptoms. rehabilitation. rehabilitation. BRONCHODILATORS  MOA of 1 bronchodilators 2 Bronchiole smooth muscle tone and mucous production are under the control of the autonomic nervous Therefore want drugs that system increase sympathetic tone and/or decrease Sympathetic activation – parasympathetic tone bronchodilation Parasympathetic activation – bronchoconstriction and increased secretion of mucus  Sympathomimetic Bronchodilators Sympathetic activation by stimulation of adrenergic receptors which increases the intracellular concentration of the nucleotide “cyclic AMP” Cyclic AMP causes bronchodilation by inhibiting the release of the chemical mediators (histamine, leukotrienes, and prostaglandins) from mast cells (which are key contributors to bronchoconstriction and inflammation in conditions like asthma.) AKA: B2 Agonists Bronchodilators  cont The sympathetic nervous system plays a key role in regulating bronchial smooth muscle tone by activating β2-adrenergic receptors on the bronchial smooth muscles. When stimulated (e.g., by drugs like beta-agonists such as albuterol or salbutamol), these receptors trigger a cascade of intracellular events that lead to an increase in cyclic AMP (cAMP).  Role of Cyclic AMP (cAMP) cAMP is a secondary messenger that plays a crucial role in various cellular processes, including bronchodilation. When β2-adrenergic receptors are activated, an enzyme called adenylyl cyclase converts ATP (adenosine triphosphate) into cAMP. Elevated levels of cAMP within bronchial smooth muscle cells lead to muscle relaxation, or bronchodilation, making it easier to breathe by widening the airways.  Xanthine Derivative Bronchodilators Xanthine drugs inhibit the enzyme phosphodiesterase that normally inactivates cyclic AMP Thus increasing the activity of cyclic AMP which results in bronchodilation *cyclic AMP lead to muscle relaxation, or bronchodilation, Activity of these drugs has only been demonstrated at very high doses and absorption/metabolism is patient dependent  Xanthine Derivative Bronchodilators Why not commonly used? Xanthine derivatives, particularly theophylline, require higher doses to reach therapeutic levels that are effective in causing bronchodilation Narrow Therapeutic Index: theophylline is 10–20 µg/mL, but doses above this can quickly lead to toxicity, including side effects like nausea, vomiting, arrhythmias, and seizures. The absorption of xanthine derivatives can vary greatly depending on the patient’s gastrointestinal tract and the formulation used. Factors such as food intake, gastric acidity, and the presence of other medications can affect how well the drug is absorbed. Smokers: Patients who smoke tend to have increased clearance of theophylline, meaning they may require higher doses. Liver Disease or Heart Failure: Patients with impaired liver function or heart failure may have slower clearance of the drug, increasing the risk of toxicity. Sympathomimetic Bronchodilators An Introduction to Child Psychology  Beta 1 receptors - 01. increases heart rate and strength of heart Adrenergic contraction Receptors Beta 2 receptors - dilation of blood vessels, bronchodilation, relaxation of smooth muscle 02. walls in digestive and urinary visceral organs, stimulates secretion of resin, which in turn increases blood pressure and blood Generally speaking sympathetic volume. activation occurs by stimulation of adrenergic receptors. 03. Alpha 1 receptors - Lorem ipsum dolor sit amet, consectetur adipiscing elit, sed do eiusmod tempor constrict blood vessels incididunt ut labore et dolore magna aliqua. There are four adrenergic receptors: Ut enim ad minim veniam, quis nostrud and visceral organ exercitation ullamco laboris nisi ut aliquip Beta 1, Beta 2, Alpha 1, and Alpha 2. ex ea commodo consequat. sphincters Alpha 2 receptors - Lorem ipsum dolor sit amet, consectetur 04. adipiscing elit, sed do eiusmod tempor inhibits release of incididunt ut labore et dolore magna aliqua. norepinepherine from Ut enim ad minim veniam, quis nostrud exercitation ullamco laboris nisi ut aliquip adrenergic terminals ex ea commodo consequat.  Adrenergic Receptors ALPHA 1 BETA 1 Location: vascular smooth muscle, bladder, and the eye Location: heart and kidneys. Functions: increases heart rate & Functions: vasoconstriction, increased blood contractility & blood pressure pressure, dilation of the pupil, contraction of the bladder neck ALPHA 2 BETA 2 Location: peripherally on certain blood vessels Location: lungs and uterus and pancreas, presynaptically in CNS Functions: bronchodilation, relaxation of Functions: inhibits the release of uterine smooth muscle, vasodilation in norepinephrine, leading to decreased skeletal muscle (greather physical strength) sympathetic outflow, sedation, and analgesia.  Alpha and Beta Adrenergic Agonists EPINEPHRINE ( EpiPen) stimulates all beta and alpha receptors onset is immediate and duration is short acting since not selective for lungs, must watch our for systemic adverse effects tachycardia, CNS stimulation, and renin secretion used usually only in emergency situations (anaphylaxis) Dosage Forms: allergac? (came off the market due to issues, came back but no one used it anymore) injection solution  Beta Adrenergic Agonists (non- selective) ORCIPRENALINE (Alupent) non-selective beta agonist (affects both beta 1 and beta 2 receptors) ratio of bronchodilating effects to cardiac stimulation is favorable at usual doses short-acting beta-2 adrenergic agonist (SABA). ONSET: less than 5 minutes if inhaled duration 3-4 hours ADVERSE EFFECTS include vasodilation, tachycardia, CNS stimulation, metabolic alterations (increase blood sugar) recently discontinued as single ingredient product  Beta 1 and Beta 2 β2-adrenergic receptors: Primarily found in the lungs, where their activation causes bronchodilation (relaxation of smooth muscles in the airways), leading to easier breathing. β1-adrenergic receptors: Mainly located in the heart, where stimulation leads to increased heart rate and contractility, causing potential cardiac stimulation "favorable at usual doses" means that at commonly prescribed doses, these drugs are designed to produce more bronchodilation (desired effect) relative to cardiac stimulation (undesired side effect) at higher doses, non-selective beta-agonists may cause more pronounced cardiac stimulation, potentially leading to side effects such as tachycardia or arrhythmias. For this reason, selective β2-agonists (e.g., albuterol) are preferred in many cases, as they provide bronchodilation with less impact on the heart.  Beta-2 Adrenergic Agonists (selective) Shorter acting (Rescue or Reliever) 1. SALBUTAMOL (Ventolin) (albuterol) 2. TERBUTALINE (Bricanyl) INDICATION symptomatic relief and prevention of acute bronchospasm due to asthma or COPD prevention of exercise induced bronchospasm ADVERSE EFFECTS: vasodilation tremor tachycardia DOSAGE FORMS: oral inhaler - onset: under 15 minutes - duration: 4-8 hours, depending on drug  LONGER ACTING (CONTROLLER OR Beta-2 Adrenergic MAINTENANCE) Agonists FORMOTEROL + budensonide -Symbicort used in treatment and prevention of symptoms of reversible obstructive airway disease in patients 6 or (selective) older Onset: under 5 minutes Duration: 12 hours Adverse Effects: headache, tremor, palpitation found primarily in the lungs, specifically in the bronchial smooth muscle, as well as in the uterus, blood vessels, and skeletal muscle. SALMETEROL + fluticasone - Advair Diskus used for maintenance treatment for patients with breakthrough symptoms not controlled by corticosteroids drugs that specifically target Beta-2 receptors and requiring regular use of short acting bronchodilator to provide bronchodilation with minimal Onset: 10-20 minutes stimulation of Beta-1 receptors (which are found Duration:12 hours mainly in the heart and affect heart rate). Adverse Effects: headache, tremor, palpitation This selectivity helps to reduce side effects like IDACATEROL - Onbrez® Breezhaler® newest on market, longer lasting, dosed once daily increased heart rate or tremors, which can occur if Beta-1 receptors are activated. provides long-lasting bronchodilation. It’s not typically used for acute symptoms or asthma, but rather for long-term management of COPD. Xanthine Derivative Bronchodilators Theophylline Products (Xanthines) Theophylline/oxtriphylline/aminoph ylline  INFORMATION a class of drugs used to treat respiratory conditions such as asthma and chronic obstructive pulmonary disease (COPD). They work by relaxing the smooth muscles of the airways, reducing bronchospasm, and improving airflow. These drugs are derivatives of xanthine, a chemical found in caffeine and theobromine. MOA: inhibiting the enzyme phosphodiesterase, which increases cyclic AMP levels, leading to bronchodilation. Also have mild anti-inflammatory effects and improve diaphragmatic contractility Xanthine derivatives are less commonly used now due to their narrow therapeutic range and potential for side effects, with newer medications (like beta-2 agonists and muscarinic antagonists) often being preferred. Blood levels need to be monitored with theophylline to avoid toxicity.  THEOPHYLLINE - Uniphyl®, Theo-24®. AMINOPHYLLINE (85% theophylline) - injections OXTRIPHYLLINE (65% theophylline) - oral tablets for symptomatic treatment of reversible bronchospasm associated with COPD (sometimes used for asthma) High toxicity and serum levels vary due to patient factors and must be carefully adjusted to target range oral tablets/capsules (extended-release) or IV injections (no inhaler form) many DRUG INTERACTIONS due to liver metabolism Blood levels can be affected by other drugs Cimetidine/erythromycin/fluoroquinolone antibiotics and verapamil increase theophylline levels Rifampin (TB), carbamazepine (Tegretol - seizures) and phenytoin (Dilantin - seizure) decrease theophylline levels Adverse Effects: n/v (Nausea/Vomiting) , nervousness, insomnia, arrhythmias, headache, tremors, convulsions Anticholinergic Bronchodilators classified into two categories: Short-Acting Muscarinic Antagonists (SAMA) and Long-Acting Muscarinic Antagonists (LAMA).  Anticholinergic Bronchodilators Mechanism of Action Not widely used to treat asthma, focused on adult COPD 01 03 Act by decreasing the Block the action of acetylcholine resulting in decreased levels of intracellular 02 intracellular concentration on “cyclic GMP” which is a parasympathetic mediator Decreased cyclic GMP that causes mucous cyclic GMP results in blocking the production and release of chemical bronchoconstriction mediators from mast cells and thus no broncoconstriction  Cyclic AMP and Cyclic GMP in relation to bronchodilation AMP: inhibit the release of chemical mediators (want to increase this) (xanthine) GMP: promote the release of chemical mediators (want decrease this) (anticholinergic)  ANTICHOLINERGIC BRONCHODILATOR SHORT ACTING LONG ACTING TIOTROPIM - Spiriva derived from atropine IPRATROPIUM - Atrovent UMECLIDINIUM - Incruse® Ellipta used for maintenance treatment of GLYCOPYRRONIUM - Seebri bronchospasms in COPD ACLIDINIUM - Tudorza adverse effects include drying of mouth and upper respiratory passage, headache, blurred vision, tremor, glaucoma, mydriasis Dosage Forms: Alternative for patients inhaler aerosol experiencing tremors or Delayed onset of short-acting drugs tachycardia from B2- action compared to agonists B2-agonists inhaler powder Adjunct in therapy for long acting drugs two methods of Longer effect than bronchodilation B2-agonists typically with beta 2 nebulizer solutions Atrovent nebules  Leukotriene Receptor part of the immune response and play a significant role in inflammatory processes, particularly in the lungs. They are activated by leukotrienes. When leukotrienes bind to these receptors, they trigger inflammatory responses, leading to bronchoconstriction, increased vascular permeability, and mucus secretion. Leukotriene Receptor Antagonists MOA MONTELUKAST - Singulair Interferes with the prostaglandins (leukotrienes) block the receptors where leukotrienes bind & cause effects Leukotrienes cause bronchoconstriction, stopping them, stops bronchoconstriction Used for prophylaxis and chronic treatment of asthma (and allergies) also indicated for use in prevention of exercise induced bronchoconstriction generally well tolerated Dosage Form: tablet Other therapies  colytics Mu N-ACETYLCYSTEINE - Mucomyst given by inhalation breaks down mucous lining bronchioles adjunctive therapy in COPD with bronchodilator as tends to be irritating to respiratory tract and may cause bronchospasm reserved for in hospital use, not commonly used for ambulatory patients  torants Expec GUAIFENESIN - Robitussin Encourages the production of respiratory tract secretions while reducing their viscosity allowing secretions to be expelled more easily by cilia and cough No primary role in the treatment of Asthma/COPD More commonly used in cough and cold preparations Dosage Form: syrup, tablets, REVIEW  bronchodilators Bronchodilator medicines open up the airways (breathing tubes) in your lungs. When your airways are more open, it’s easier to breathe. Doctors may prescribe more than one kind of bronchodilator to treat COPD. There are two main types of bronchodilators that come in inhalers: Beta-2 agonists: Anticholinergics: 1. salbutamol (Ventolin ® or Airomir ®) SA 1. ipratropium bromide (Atrovent ®) - SA 2. terbutaline (Bricanyl ®) SA 2. tiotropium (Spiriva ®) 3. formoterol (Oxeze ® Foradil ®) LA 3. glycopyrronium (Seebri ®) 4. salmeterol (Serevent ®) LA 4. aclidinium (Tudorza ®) 5. indacterol (Onbrez ®) LA 5. umeclidinium (Incruse)  bronchodilators Rapid-onset bronchodilators (also called quick-relief medicines) act quickly and start to relieve shortness of breath within minutes. They are often used as needed, to help relieve sudden shortness of breath. Quick-relief medicines usually come in a blue puffer. Some rescue medicines are short-acting and last for 4-6 hours (like Ventolin ® or Bricanyl ®). Some are long-acting and last for up to 12 hours (like Oxeze ®). Slow-onset bronchodilators take longer to act. Some last for 4 to 6 hours (like Atrovent ®), and some last up to 12 hours (like Serevent ®). Some slow-onset bronchodilator lasts for 24 hours (Spiriva ®).  d ila to rs Bronc ho l ass es : 2m ain c 1. Beta-Adrenergic Sympathomimetic Drugs = B2 Agonists Short Acting Beta 2 Agonists (SABA) Long Acting Beta 2 Agonists (LABA) SHORT ACTING LONG ACTING salbutamol - Ventolin formoterol - Symbicort terbutaline - Bricanyl salmeterol - Advair Diskus idacaterol - Onbrez Breezhaler  d ila to rs Bronc ho l ass es : 2m ain c 2. Anti-cholinergic Drugs = Muscarinic Antagonists Short Acting Muscarinic Antagonists (SAMA) Long Acting Muscarinic Antagonists (LAMA) SHORT ACTING LONG ACTING Ipratropium - tiotropim - Spirvia umeclidinum - Incruse glycopyrronium - Seebri aclidinum- Tudroza  bin at io n Com rap ie s The Determine the two active ingredients in each What class are they from? Why would they be combined together? Combivent Duaklir Ultibro Symbicort Advair - fluticasone (steriod) + formoterol (long-acting)  b i v e n t C om ACTIVE INGREDIENTS: Ipratropium bromide - (SAMA) Albuterol/Salbutamol - (SABA) RATIONALE FOR COMBINATION: Ipratropium is an anticholinergic medication that works by blocking the action of acetylcholine on muscarinic receptors, leading to bronchodilation. Albuterol is a short-acting beta-agonist (SABA) that stimulates beta-2 adrenergic receptors, causing the muscles around the airways to relax. The combination can: provide better control of bronchospasm act relatively quickly, provide rapid relief from acute symptoms of bronchospasm, making them useful during exacerbations of COPD or asthma. Dukalir ACTIVE INGREDIENTS: Used for the maintenance treatment of COPD. It is Aclidinium bromide (LAMA) not intended for the relief of acute bronchospasm. Formoterol fumarate (LABA) RATIONALE FOR COMBINATION: Aclidinium: Blocks the action of acetylcholine, which can cause airway constriction, leading to bronchodilation. Formoterol: Stimulates beta-2 adrenergic receptors, leads to airway dilation and improved airflow. The combination can: Long lasting effects: providing sustained bronchodilation for up to 24 hours with regular use. enhance symptom control  l t i b r o U ACTIVE INGREDIENTS: Glycopyrronium (LAMA) Indacaterol (LABA) RATIONALE FOR COMBINATION: Indacaterol: Stimulates beta-2 adrenergic receptors, resulting in relaxation of the airway smooth muscles, which helps to improve airflow. Glycopyrrolate: Prevents bronchoconstriction by blocking muscarinic receptors, which reduces airway resistance and improves lung function. The combination can: enhanced and prolonged bronchodilation beneficial in managing COPD symptoms  b i c o r t s ym ACTIVE INGREDIENTS: Budesonide (Inhaled Corticosteroid) Formoterol (LABA) RATIONALE FOR COMBINATION: Budesonide: Works by inhibiting the inflammatory response in the airways, reducing swelling and mucus production, making it easier to breathe. Formoterol: Stimulates beta-2 adrenergic receptors, leading to bronchodilation, which helps to improve airflow and relieve symptoms of bronchospasm. The combination can: addresses both inflammation and airway constriction Patients may experience fewer asthma attacks or COPD exacerbations with regular use.