Altered Respiratory Functions (Part-3) - Pathophysiology Sultan Qaboos University PDF

Sultan Qaboos University College of Nursing 2024, Fall Semester Pathophysiology Altered Respiratory Functions (Part-3) Dr. Joshua Muliira RN, DNP Associa...

Sultan Qaboos University College of Nursing 2024, Fall Semester Pathophysiology Altered Respiratory Functions (Part-3) Dr. Joshua Muliira RN, DNP Associate Professor  Objectives Students are expected to: Describe the triggers, pathophysiology, and manifestations of an acute asthma attack. Describe the pathogenesis and manifestations of COPD. Differentiate among causes and manifestations of chronic bronchitis and emphysema. Obstructive Lung Diseases ASTHMA COPD  Obstructive Airway Disorders Caused by increase resistance to airflow Parasympathetic stimulation, through cholinergic receptors and vagus nerve produce bronchoconstriction Sympathetic stimulation through B2- adrenergic receptors produces bronchodilation Bronchial smooth muscle also response to the inflammatory mediator (Histamine, Cytokines) which produce bronchoconstriction  Definition Asthma: involves periodic episodes of severe but reversible bronchial obstruction in persons with hypersensitive or hyperresponsive airways. Frequent repeated attacks of acute asthma may lead to irreversible damage in the lungs and the development of chronic asthma (COPD).  Etiology/Precipitating Factors Exact cause is unknown Asthma “trigger” result in hypersensitivity reactions and trigger the inflammatory response. Exercise n s e rg lle A Irr Pollen ita tsn Cold air Gases  Bronchial Asthma In asthma many cells and cellular elements play a role in particular: mast cell, B & T lymphocytes, & epithelial cells Asthma categorized into extrinsic asthma and intrinsic asthma 1. Extrinsic (atopic) asthma Initiated by type 1 hypersensitivity reaction induced by exposure to extrinsic antigen or allergen. Most common in childhood and adolescence Among allergens are house dust mite allergens, cockroach, pollen, allergens, animal dander, fungus  Bronchial Asthma 2. Intrinsic (Nonatopic) asthma Include hyperventilation, cold air, exercise, emotional upset, aspirin and other NSAID and gastroesophageal reflux Exercise induced asthma may be caused by loss of heat and water from tracheobronchial tree and loss of warming and humidification  Bronchial Asthma Inhaled irritants such as tobacco smoke and strong odors thought to induce asthma by the way of irritant receptors and a vagal reflex Emotional factors produce bronchospasms by the way of vagal pathway and can increase air responsiveness to other triggers Reflux of gastric secretion act as bronchospastic trigger  Pathophysiology Early-phase (10-20 minutes after exposure)  Pathophysiology Late-phase Early-phase (6-24 hours after exposure) (10-20 minutes after exposure) Pathophysiology (Acute episode)  Pathophysiology Early-phase response Allerge n Sensitizing IgE Mast cells Degranulation Bronchospasm Release of histamine, IL, Prostaglandins Infiltration of inflammatory cells Airflow Release cytokines, IL, and limitati other inflammatory on mediators Late-phase Increased response Airway inflammation airway responsivenes s Edema Epithelial injury Impaired mucociliary function Asthma Inflammatory mediators lead to airway inflammation, edema of the mucous lining of the airways, bronchospasm, and impaired ability to clear secretions.  Clinical manifestations In times of exacerbation, hyperreactivity, and inflammation in the airways (acute asthma attack): Wheezing, Breathlessness, Chest tightness Excessive sputum production, Coughing Using of accessory muscles, Fatigue Anxiety, dyspnea  tachypnea hyperventilation Respiratory alkalosis: Initially due to hyperventilation Respiratory acidosis: In time due to air trapping Hypoxia  Asthma: Treatment General measures – Skin tests for allergic reactions – Avoidance of triggering factors – Good ventilation of environment – Swimming and walking – Use of maintenance inhalers or drugs Measures for acute attacks – Controlled breathing techniques – Inhalers Bronchodilators – Glucocorticoids (beclomethasone)  COPD Group of chronic respiratory disorders Causes irreversible and progressive damage to lungs Debilitating conditions that may affect ability to work May lead to the development of cor-pulmonale Respiratory failure may occur.  Emphysema An irreversible enlargement of the air spaces beyond the terminal bronchioles (alveoli), resulting in destruction of the alveolar walls and obstruction of airflow.  Etiology The most common cause of COPD is smoking Genetic factor – Deficiency of alpha1-antitrypsin (AAT) Pathophysiology Smoki Attraction of inflammatory ng cells Release of elastase Action inhibited by α- antitrypsin Decreased Inherited α- α-antitrypsin antitrypsin activity deficiency Destruction of elastic fibers in lungs Emphysem a Pathophysiology  COPD: Emphysema (Cont.) Breakdown of alveolar wall results in: – Loss of surface area for gas exchange – Loss of pulmonary capillaries – Loss of elastic fibers – Altered ventilation-perfusion ratio – Decreased support for other structures Fibrosis – Narrowed airways – Weakened walls – Interference with passive expiratory airflow  COPD: Emphysema (Cont.) Progressive difficulty with expiration – Air trapping and increased residual volume – Overinflation of the lungs – Fixation of ribs in a respiratory position that increases anterior-posterior diameter of thorax (barrel chest) – Flattened diaphragm (on radiographs)  Clinical manifestations The onset of emphysema is insidious Dyspnea Hyperventilation with prolonged expiratory phase Hyperinflation – Leading to a “barrel chest” Anorexia and fatigue = weight loss  Diagnostic Tests & Treatment Diagnostic tests – Pulmonary function tests – Chest radiography Treatment – Smoking cessation – Oxygen – Appropriate breathing techniques (e.g. pursed-lip breathing)  Emphysema (Pink Puffers) Manifestations: Hyperventilation Breathlessness Destruction of alveolar sacs leads to damaged pulmonary capillary bed Using Pursed accessory Barrel-chest: hyperinflation of lips muscles  Chronic Bronchitis (CB) CB = airway obstruction of the major and small airways Chronic irritation from smoking & recurrent infections Hypertrophy of the submucosal glands in the trachea and bronchi  Etiology Cigarette smoking Living in an urban or industrial area Exposure to environmental pollutants that irritate the airways. Pathophysiology Chronic irritation (e.g. smoking) Hyperplasia of the Narrowing of Squamous bronchial lumen metaplasia mucous glands Reduced cilia Increased action mucus Obstruction production Reduced clearance of microorganisms Increased Productive Dyspnea respiratory cough infections  Clinical Manifestations The clinical manifestations of chronic bronchitis are often similar to emphysema because the two conditions often occur simultaneously. Chronic productive cough (purulent sputum) Dyspnea Wheezing and crackles upon auscultation Hypoxemia, hypercapnia and CYANOSIS  Diagnostic Tests & Treatment Diagnostic tests Treatment – History of smoking + – Smoking symptoms cessation (productive cough – Bronchodilato over a period of 3 months) r therapy – ABG (hypoxemia and – Steroid anti- hypercapnia) inflammatory – Blood tests drugs (polycythemia) – Supplemental – Pulmonary function oxygen test therapy  Chronic Bronchitis (Blue Bloaters) Manifestations: Increased secretion Increased obstruction cyanosis Pulmonary capillaries are undamaged Cyanosi Edema s  Nursing Considerations Urge the patient to stop smoking Encourage to avoid respiratory irritants. Review the use of any bronchodilators and antibiotics the patient is taking