Lower Respiratory Disorders PDF
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This document appears to be student notes covering lower respiratory disorders like asthma, emphysema and COPD. This resource details the various diseases of the lower respiratory tract and their related treatments, and includes discussions on pathophysiology, clinical manifestations, and medications.
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LOWER RESPIRATORY DISORDERS Patho/Pharm I Respiratory System Review Main function of Respiratory System is:??? How is this accomplished: Ventilation Diffusion Perfusion Conducting Airways Composition Alveoli destruction is irreversible...
LOWER RESPIRATORY DISORDERS Patho/Pharm I Respiratory System Review Main function of Respiratory System is:??? How is this accomplished: Ventilation Diffusion Perfusion Conducting Airways Composition Alveoli destruction is irreversible Two Types of Cells: Type I Alveolar, Type II Alveolar Pulmonary Circulation: Facilitates Gas Exchange Respiratory System Review 102 02 Diseases of the Lower Respiratory Tract Asthma Emphysema COPD (Chronic Obstructive Chronic Bronchitis Pulmonary Disease) Pneumonia Tuberculosis Asthma Pathophysiology to baseline wheezing goes back Recurrent and reversible shortness of breath Allergic Cascade: Following exposure to an allergen, a series of reactions will occur 1. Sensitization to an allergen Initial exposure to an allergen T cells stimulate B cellsmemorycells B cells develop into plasma cells attained Plasma cells produce IgE antibodies (targeted to that specific allergen) IgE binds to receptors on mast cells Asthma Pathophysiology 2. Early phase response upon re-exposure to an allergen Ige of mast cells binds to the allergen, cross-linking with the IgE When enough cross-linking occurs the mast cells explode releasing mediators (Histamines, prostaglandins, leukotrienes) These immune mediators cause: Bronchoconstriction, vasodilation, increased capillary permeability occurs within several minutes I fluidmovingintotissues 3. Late phase response to an allergen Begins at the same time as early phase response See worsening symptoms 3-10 hours later Last for 24 hours May involve eosinophils I increased Proffinfallergiraction Pathophysiology of Asthma Airflow obstruction is related to: Contraction of airway smooth muscle Thickening of airway wall due to cellular edema Plugging of the airways with mucous and debris Obstruction in large airways leads to air flow limitation and decreased flow rates. Obstruction in the small airways leads to airway closure and air-trapping hyperinflation. Alveolar ducts/alveoli remain open, but airflow to them is obstructed Factors causing obstruction 100 back to normal reversible Asthma Types of asthma Exercise induced exaceraShma Intrinsic Respiratory Infections Gender Nasal/Sinus problems Genetic atopy postnasaldrip Extrinsic irritates bronchioleairways Allergens Air Pollutants Occupational Forms Drug and Food Additives Clinical Manifestations Unpredictable and variable Recurrent episodes of wheezing, breathlessness, cough and tight chest May be abrupt or gradual Lasts minutes to hours Shortened breath in Expiration may be prolonged Prolonged expiration Inspiration-expiration ratio of 1:2 to 1:3 or 1:4 Air takes longer to move out Clinical Manifestations Wheezing is unreliable to gauge severity Severe attacks may have no audible wheezing Usually begins upon exhalation Difficulty with air movement can create a feeling of suffocation. Patient may feel increasingly anxious An acute attack usually reveals signs of hypoxemia Restlessness, Anxiety, inappropriate behavior, increase pulse and blood pressure Asthma Complications Status asthmaticus Prolonged asthma attack that does not respond to typical drug therapy May last several minutes to hours Medical emergency intubation and mechanical ventilation Chronic Bronchitis Definition: Chronic Productive cough for three months in each of two successive years in a patient whom other causes of chronic cough have been excluded. Never goes back to baseline Permanent structural damage Irreversible Continuous inflammation of the bronchi and bronchioles Often occurs as a result of prolonged exposure to bronchial irritants toxics exsmoking Increase in number of goblet cells with damaged cilia Mphation Emphysema Definition: Abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls. respitates Airtrapping inappsed caused by inflammation COPD: Description Chronic bronchitis Chronic inflammation of bronthiole Emphysema destruction of avioli sais Risk factors Cigarette smoking Occupational chemicals and dust Air pollution Generally progressive00 Airflow limitation not fully reversible Abnormal inflammatory response of lungs to noxious particles or gases Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 0 COPD Smoking effects on respiratory tract Increased production of mucus Hyperplasia of mucous glands cells belome larger Lost or decreased ciliary activity COPD can develop with intense or prolonged exposure to Dusts, vapors, irritants, or fumes High levels of air pollution Fumes from indoor heating or cooking with fossil fuels COPD Pathophysiology Defining features Irreversible airflow limitations during forced exhalation due to loss of elastic recoil Airflow obstruction due to mucous hypersecretion, mucosal edema, and bronchospasm Primary process is inflammation. Inhalation of noxious particles Mediators released cause damage to lung tissue. Airways inflamed Parenchyma destroyed 0 COPD Pathophysiology Supporting structures of lungs are destroyed. Air goes in easily, but remains in the lungs. Bronchioles tend to collapse. Causes barrel-chest look air trapping Pulmonary vascular changes Blood vessels thicken. Surface area for diffusion of O2 decreases. hypoxicstate 0 COPD Pathophysiology Common characteristics Mucous hypersecretion Dysfunction of cilia Hyperinflation of lungs Gas exchange abnormalities Commonly, emphysema and chronic bronchitis coexist. Distinguishing symptoms can be difficult with co- morbidities. 0 COPD Clinical Manifestations Develops slowly Diagnosis is considered with Cough Sputum production clear intention yellowgreen Dyspnea Exposure to risk factors 0 COPD Clinical Manifestations Dyspnea usually prompts medical attention. Occurs with exertion in early stages Present at rest with advanced disease Causes chest breathing Use of accessory and intercostal muscles increased work of breath metabolicallydemanding Inefficient Characteristically underweight with adequate caloric intake Chronic fatigue 0 COPD Clinical Manifestations Physical examination findings Prolonged expiratory phase Wheezes Decreased breath sounds ↑ Anterior-posterior diameter barrel chest Bluish-red color of skin Cyanosis hypoxinstate compensate forhypoxia Overproduition of RBC to. 0 Medications Used to Treat Asthma and COPD Bronchodilators 1.Beta2-adrenergic agonists 2. Anticholinergics 3. Xanthine Derivatives Antinflammatory Leukotriene receptor antagonists Corticosteroids New Asthma Medications Bronchodilators: Beta2Agonists Mechanism of Action: Stimulation of beta2 adrenergic receptors in the bronchial smooth relaxatishing muscle throughout lungs causing bronchodilation Three subtypes of drugs(Based on Selectivity for receptors) Nonselective adrenergic drugs greater side effects Nonselective beta-adrenergic drugs Selective beta2 drugs Bronchodilators: Beta-Agonists attack thatment Short-acting inhalers/nebulizers: (SABA) rapid onset albuterol (Ventolin)(Proventil) (PO, Inhaled) Short livid PRNmed levalbuterol (Xopenex) (Inhaled) Rescue Inhalers terbutaline (Brethine) (PO, SQ, Inhalation) Long-acting (LABA) (Inhalation only) Longonset Long lasting Salmetrol (Serevent) I Formoterol (Foradil) Arformoterol (Brovana) Maintenance manage drug therapy Bronchodilators: Beta-Agonists Indications: brontaxation Relief of bronchospasm related to asthma, bronchitis and other pulmonary diseases Used in treatment and prevention of acute and chronic attacks depending on their onset of action. short vs long atting Additional indications: hypotension, shock, uterine relaxation. Bronchodilators: Beta2-Agonists Adverse Effects Tremors Tachycardia Vascular headache Insomnia, Restlessness Nursing Implications-Beta2- Agonists Beta-agonist derivatives Albuterol, if used too frequently , loses its beta2- Ain'tused ONLYPRN specific actions at larger doses As a result, beta1 receptors are stimulated, causing nausea, increased anxiety, palpitations, tremors, and increased heart rate Ensure that patients take medications exactly as prescribed, with no omissions or double doses. Inform patient to report insomnia, jitteriness, restlessness, palpitations or chest pain. Bronchodilators (Anticholinergics): Mechanism of Action Bronchial tree contains Acetylcholine which causes bronchial constriction and narrowing of the airways Anticholinergics bind to the ACh receptors, preventing ACh from binding. Results: Indirect airway dilation, reduction of secretions Main indication: Prevention of bronchospasm associated with COPD, allergen and exercise induced asthma. medication Daily management Bronchodilators: Anticholinergics ipratopium bromide (Atrovent) tiotropium (Spiriva) Aclidinium (Tudorza) Umeclidinium and vilanterol (Anoro Ellipta) Routes available: (Inhaler or Nebulizer) Slow and prolonged action Used to prevent bronchoconstriction NOT used for acute asthma exacerbations Anticholinergics: Side Effects Nursing Implications Dry mouth or throat Instruct patient to rinse Hoarseness mouth after Nasal Congestion medication administration Headache Coughing Anxiety Heart Palpitations Urinary retention Bronchodilators: Xanthine Derivatives Example: theophylline (Theo-Dur, Elixohyliin) Routes Available: Oral, rectal and Intravenous- Emergency only Mechanism of Action: Causes relaxation of bronchial smooth muscle resulting in bronchodilation by increasing camp. Result: Smooth muscle relaxation Bronchodilation Increased airflow Xanthine Derivatives: Indications Dilation of airways in asthmas, chronic bronchitis and emphysema Adjunct drug in the management of COPD Not used as frequently because of potential for drug interactions and variables related to drug levels in the blood (toxicity) Xanthine Derivatives: Adverse Effects Nausea, vomiting, anorexia, GERD Dysrhythmia Seizures SDOH Relatively cheap Albuterol -without insurance between $30 and $60 Albuterol - with insurance between $5 and $50 depending on copay Ipatroprium bromide-without insurance $200 Theophylline – without insurance $100 per month Prescription required, access to provider Exposure to pests, mold, air pollution (including secondhand smoke) Anti-inflammatory Medications Leukotriene Receptor Antagonists (LTRAs) Acts on eosinophil reaction Route: PO montelukast (Singulair) (once daily dosing) zafirlukast (Accolate) zileuton (Zyflo) Indications: Long term therapy of asthma in adults and children. Prevention of exercise induced bronchospasm Management of seasonal allergies Leukotriene Receptor Antagonist: Mechanism of Action Focus on modifying the immune response Leukotrienes are substances released when a trigger (allergen) starts a series of chemical reactions in the body. Leukotrienes cause inflammation, bronchoconstriction, and mucus production. Results: coughing, wheezing, shortness of breath. Leukotriene Receptor Antagonists work by preventing leukotrienes from attaching to receptors on cells in the lungs and in circulation Leukotriene Receptor Antagonists: Adverse Effects montelukast (Singulair)- Neuropsychiatric effects in children and adolescents zafirlukast (accolate)-headache, nausea, diarrhea, liver dysfunction zileuton(Zyflo)- headache, dyspepsia, nausea, dizziness, insomnia, liver dysfunction. Leukotriene Receptor Antagonists Ensure that the drug is being used for chronic management, not acute episodes Improvement should be seen in about a week Assess liver function before beginning therapy seasonal for Teach patient to take medications every night on a allergies continuous schedule, even if symptoms improve Exception: If symptoms related to sports or exercise take two hours prior to activity Corticosteroids Anti-inflammatory properties Do not relieve symptoms of acute asthmatic attacks Oral, Inhaled, IV forms Stabilizes membrane Inhaled forms reduce systemic effects Oral: not for acute exacerbations IV: Acute asthma or COPD exac May take several weeks before full effects are seen Corticosteroids: Mechanism of Action Stabilize membranes of cells that release harmful bronchoconstricting substances These cells are called leukocytes, or white blood cells Increase responsiveness of bronchial smooth muscle to beta-adrenergic stimulation Inhaled Corticosteroids beclomethasone dipropionate (Beclovent, Vanceril) Budesonide (Pulmicort) triamcinolone acetonide (Azmacort) fluticasone (Flovent, Flonase) fluticasone and salmeterol (Advair) Indications: Treatment of bronchospastic disorders that are not controlled by conventional bronchodilators NOT considered first-line drugs for management of Inhaled Corticosteroids: Adverse Effects Pharyngeal irritation Coughing Dry mouth Oral fungal infections thrush Systemic effects are rare because low doses are used for inhalation therapy Inhaled Corticosteroids: Nursing Implications Teach patients to gargle and rinse the mouth with lukewarm water afterward to prevent the development of oral fungal infections If a beta-agonist bronchodilator and corticosteroid inhaler are both ordered, the bronchodilator should be used several minutes before the corticosteroid to provide bronchodilation before administration of the corticosteroid Inhaled Corticosteroids: Nursing Implications Teach patients to monitor disease with a peak flow meter Encourage use of a spacer device to ensure successful inhalations Teach patient how to keep inhalers and nebulizer equipment clean after uses Oral Corticosteroids Example: prednisone, prednisolone Indications: Short-term therapy following and acute asthma episode, copd exacerbation Long-term therapy for acute asthma inhaled corticosteroids Oral Corticosteroids Side Effects of long term therapy Suppression of adrenal gland function Bone loss Hyperglycemia, glycosuria Myopathy Peptic ulcer disease Infection modulating inflammatory response Fluid and Electrolyte Imbalance Intravenous Corticosteroids hydrocortisone sodium succinate (Solu-cortef) Methylprednisolone sodium succinate (Solu- mederol) Indications: Short term IV agents used for acute exacerbations of COPD and status asthmaticus. Side Effects: Similar to side effects of long-term oral therapy. Alert: Monitor patients closely when switched to inhaled steroids after receiving systemic steroids due to adrenal insufficiency Combination Medications Fluticasone/Salmeterol Inhaler Budesonide/Formoterol s Ipratropium/Albuterol- Inhalers, Nebulizers Combined inhaled corticosteroid long aiting bronchodilather SDOH Disproportionate burden of COPD occurs in people of low socioeconomic status (SES) due to differences in health behaviors, social structure, environmental exposures, tobacco use, occupations with exposure to inhalant toxins More expensive Leukotriene Receptor Antagonists $8-$30 than bronchodilators Inhaled corticosteroids $200 (without insurance) Oral steroids – starts at $5 (much cheaper than others) Newest Medications Phosphodiesterase-4 Monoclonal Antibody inhibitor (FDA (Binds to IgE limits approval 2011) release of chemical Roflumilast (Daliresp) mediators of Oral inflammation) Used for COPD Omalizumab (Xolair) exacerbations Subcutaneous every Monitor for anxiety two to four weeks and depression Antiasthmatic Monitor for often prescribed as last anaphylaxis don'twork resort if other medications Nursing Implications Encourage patients to take measures that promote a generally good state of health so as to prevent, relieve, or decrease symptoms of COPD Avoid exposure to conditions that precipitate bronchospasm (allergens, smoking, stress, air pollutants) Adequate fluid intake Compliance with medical treatment Avoid excessive fatigue, heat, extremes in temperature, caffeine Advocate for vaccinations Asthma Stepwise Guidelines 0 Nursing Implications Encourage patients to get prompt treatment for flu or other illnesses, and to get vaccinated against pneumonia and influenza Encourage patients to always check with their physician before taking any other medication, including over-the- counter medications Teach patients to take bronchodilators exactly as prescribed Ensure that patients know how to use inhalers and MDIs, and have patients demonstrate use of the devices Monitor for adverse effects Nursing Implications Perform a thorough assessment before beginning therapy, including: Skin color Baseline vital signs Respirations Jotassessment, including pulse oximetry breathing Respiratory Sputum production Allergies History of respiratory problems Other medications Nursing Implications Monitor for therapeutic effects Decreased dyspnea Decreased wheezing, restlessness, and anxiety Improved respiratory patterns with return to normal rate and quality Improved activity tolerance Decreased symptoms and increased ease of breathing Inhalers: Patient Education Ensure that the patient is able to self-administer Provide demonstration and return demonstration Ensure that the patient knows the correct time intervals for inhalers Provide a spacer if the patient has difficulty coordinating breathing with inhaler activation Ensure that the patient knows how to keep track of the number of doses in the inhaler device Patient Education