Presentation on Respiratory Disorders

Respiratory Disorders Chapter 19 Pgs 310-360 Homework Assignment • • • • • Due Tuesday Oct 18 It does NOT have to be typed! You may work in groups Answers MUST be in your own words Case Study A – a, b,c, d, f, g, h, o • Case Study B – a, c, g, h, i, j • Case Study C – a, b, g, h, i Overview • Diagnostic Tests • General Manifestations of Respiratory Disease • Infectious Diseases – Upper respiratory tract infections • Common cold • Sinusitis – Lower respiratory tract infections • RSV • Pneumonia • Obstructive Lung Diseases – Lung Cancer – Asthma • Chronic Obstructive Pulmonary Disease (COPD) – Emphysema – Chronic Bronchitis Diagnostic Tests • • • • • • • Spirometry Arterial blood gas determination Oximeters Exercise tolerance Radiography Bronchoscopy Culture, sensitivity tests General Manifestations of Respiratory Disease • Sneezing • Coughing – Irritation – Controlled by medulla – Constant, dry unproductive vs. productive cough • Sputum – – – – – Mucus discharge Yellowish-green Rusty, dark-colored Thick, sticky Hemoptysis Manifestations • Breathing patterns and characteristics – Kussmaul respiration – Labored respiration, prolonged inspiration/expiration times – Wheezing – Stridors • Breath sounds – Rales – Rhonchi – Absence Manifestations • Dyspnea – Severe – Orthopnea – Paroxysmal nocturnal dyspnea • • • • • Cyanosis Pleural pain Friction rub Clubbed fingers Changes in ABG (arterial blood gases – Hypoxemia  inadequate oxygen in blood – Hypoxia  inadequate oxygen supply to cells Causes of Hypoxia • • • • • Low RBC, Hb Circulation impairment Excessive release of oxygen from RBC Impaired respiratory function CO poisoning Upper Respiratory Tract Infections: Common Cold (Infectious Rhinitis) • • • • Viral (rhinovirus) Spread thru respiratory droplets Highly contagious Initially mucous membranes of nose, pharynx swollen, increased secretions • Signs – – – – – Nasal congestion and watery discharge Mouth breathing Change in tone of voice Sore throat, headache, slight fever Cough Common Cold • Infection, inflammation can spread – Laryngitis – Bronchitis • Treatment is symptomatic – Acetaminophen – Decongestant – Antihistamine – Humidifiers – Are antibiotics prescribed? Secondary Bacterial Infections Sinusitis • Secondary bacterial infection • Obstruct drainage in 1 or more paranasal sinuses • Common causative organisms – Pneumococci – Streptococci – Haemophilus influenzae • Exudate accumulates • Signs – Nasal congestion, fever, sore throat • Diagnosis confirmed by radiograph, transillumination • Decongestants, analgesics • Antibiotics Lower Respiratory Tract Infections: Bronchiolitis (RSV Infection) • • • • • • 2-12 month Caused by syncytial virus Transmitted by oral droplet Predisposing factors (asthma, smoking) Causes necrosis and inflammation of small bronchi and bronchioles Signs – – – – – – Wheezing and dyspnea Rapid, shallow respirations Cough Rales Chest retractions Fever • Treatment – Supportive and symptomatic Pneumonia • Primary acute or secondary • Risk following aspiration, inflammation in lung • Transmission – Inhaling virus – Resident bacteria spreading along mucosa – Aspiration in secretions Classification of the Pneumonias • Causative agent – Virus, bacteria, fungus – Lobar is typically bacterial • Pneumococcus • Anatomical distribution of lesion – Both lungs or lobar • Pathophysiologic changes – Viral  changes in interstitial tissue or alveolar septae – Pneumococcal  alveoli inflamed and fluid filled • Exudate • Epidemiologic categories – Nosocomial – Community acquired Lobar Pneumonia • Streptococcal pneumoniae, pneumococcal • Infection localized in 1 or more lobes Stages of Pneumonia • Congestion – Inflammation and vascular congestion in alveolar wall • Exudate forms in alveoli – Interferes with oxygen diffusion • Consolidation – Neutrophils, RBCs, fibrin accum in exudate • Form solid mass • RBCs break down, infection resolves – Macrophages break down exudate • Expectorated or resorbed Consolidation Pneumonia • Pleurae typically involved – Infection in pleural cavity • Emphysema – Adhesions between membranes • Manifestations – – – – – – Sudden onset Systemic signs: high fever, chills, fatigue Dyspnea, tachycardia Pleuritic pain Rales Productive cough Pneumonia • Treatment – Antibacterials (Penicillin) – Supportive measures – Pneumococcal vaccine Obstructive Lung Disease: Lung Cancer • Primary or secondary; benign rare – Primary is major cause of death • Linked with cigarette smoking • Metastases develop freq in lung b/c: – Venous return and lymph vessels bring tumor cells from distant site in body  heart  lung • Poor prognosis Normal Lung vs. Cancerous Lung Types of Lung Cancer • • • • • Bronchogenic carcinoma – Most common – Arise from bronchial epithelium Squamous cell carcinoma – Develop from epithelial lining in bronchus – Project into airway Adenocarcinomas and bronchoalveolar cell carcinoma – Found on lung periphery – Less symptomatic, more difficult to treat Small cell carcinoma – Rapidly growing; located near major bronchus – Invasive and metastize early in dev Large cell carcinoma – Found in periphery – Consist of large, undifferentiated cells – Rapid growth rate, metastize early Bronchogenic Carcinoma Lung Cancer—Pathophysiology • First change – Metaplasia, change in epithelial tissue • Smoking, chronic irritation • Reversible if irritation removed – Loss of ciliated pseudostratified epithelium • More vulnerable to irritants • Next – Dysplasia, carcinoma develop – Hard to detect Lung Cancer—Effects of Tumors • Obstruction of air flow • Inflammation • Pleural effusion, hemothorax, pneumothorax • Paraneoplastic syndrome Lung Cancer—Etiology • General stats – 173,330 new cases each year – 160,440 deaths per year • Smoking (primary and secondary) – 87% of lung cancers related to smoking – 1 out of 10 chances of developing lung cancer • Maybe a genetic factor • Occupational exposure to carcinogens • Irritant that leads to chronic inflammation – Cause cell changes • Smoking: ciliated columnar  squamous Lung Cancer—Signs and Symptoms • Insidious onset • Normally metastized before diagnosis • 4 possible categories of signs of lung cancer – Direct effects of tumor – Systemic effects of cancer – Paraneoplastic syndromes – Metastizes at other sites Lung Cancer—Early Signs (#1) • Persistent, productive cough, dyspnea, wheezing • Detection on chest X-ray • Hemoptysis • Pleural involvement • Chest pain • Hoarseness • Facial, arm edema; headaches • Dysphagia Lung Cancer (#2-4) • Systemic signs – Wt. loss, anemia, fatigue • Paraneoplastic syndrome – Signs of endocrine disorder – Depends on hormone being secreted • Signs of metastasis depends on site Lung Cancer—Diagnostic Tests • Chest X-rays • Bronchoscopy • Pulmonary function tests Lung Cancer—Treatment • Surgery on localized lesions • Chemotherapy and radiation • Poor prognosis unless tumor in early stages of development Asthma • Periodic episodes of severe but reversible bronchial obstruction • Frequency may lead to irreversible damage and COPD • 2 types – Extrinsic asthma • Acute episodes triggered by type I hypersensitivities • Onset in childhood – Intrinsic asthma • Onset during adulthood • Stimuli target hyperresponsive tissue = acute attack Asthma—Pathophysiology: Acute Attack • Both types • Bronchi and bronchioles respond to stimulus with 3 changes – Bronchoconstriction – Inflammation of mucosa with edema – Increased secretion of thick mucus in passageways • Changes may result in partial or total obstruction of airways – Interferes with oxygen supply, air flow Asthma—Pathophysiology: Extrinsic Asthma • 1st stage – Allergen reacts with IgE on previously sensitized mast cells in resp. mucosa • Release chemical mediators (histamine, prostaglandin) – Stimulates vagus nerve • Reflex bronchoconstriction • 2nd stage – Hours later – Increased leukocytes release more chemical mediators • Prolong bronchoconst and epithelial damage • Increase WBC – Obstruction, hypoxia Asthma—Pathophysiology: Partial Obstruction • • • • Small bronchi, bronchioles Air trapping with hyperinflation of lungs Air only partially expired Expiration passive – Now less force to move air out – Forced collapses bronchial wall • Even more difficult to expire • Increased residual volume – More difficult to inspire fresh air, cough Asthma—Pathophysiology: Total Obstruction • Mucus plugs completely block • Air in distal section diffuses out – Cannot be replaced • Lung in that section collapses • Both (partial and total) lead to hypoxia and hypoxemia • Status asthmaticus – Persisant severe asthma attack – Does not respond to therapy – Can be fatal • Chronic asthma and COPD may develop – Irreversible damage in lungs Asthma—Etiology • Family history of hay fever, asthma, eczema • Significant rise due to: – Sedentary lifestyles and obesity – Increased time indoors – Increased air pollution Asthma—Signs and Symptoms • • • • • • • • • Cough, dyspnea, tight feeling in chest Wheezing Rapid, labored breathing Thick, sticky mucus coughed up Tachycardia and pulse paradoxus – Pulse differs on inspiration and expiration Hypoxia Respiratory acidosis Severe respiratory distress Respiratory failure Asthma—Treatment • • General measures – Determine allergies – Avoid triggers Acute attacks – Inhalers • Bronchodilators (albuterol) • Most effective at 1st indication of attack – Controlled breathing techniques and decrease anxiety – Glucocorticoids • • Hospital care—status asthmaticus Prophylaxis and treatment of chronic asthma – Leukotrine receptor antagonists (Singulair) • Block inflammation response • Taken regularly, not effective for acute attacks – Cromolyn sodium • Inhibits release of chemical mediators from sensitized mast cells • Not effective for acute attacks Chronic Obstructive Pulmonary Disease (COPD) • Progressive tissue damage and obstruction of airways • Affect individual’s ability to work and function indep – Eventual resp failure • Leads to R CHF • Includes – Emphysema – Chronic bronchitis – Asthma Emphysema—Pathophysiology • Significant change is destruction of alveolar walls and spaces – Leads to lg, inflated alveoli • Classified by specific location of changes – Ex: Distal alveoli emphysema – Ex: Bronchiolar emphysema Emphysema—Pathophysiology: Contributing Factors • Genetic – Low alpha1-antitrypsin • Protein normally present in tissues • Inhibits action of proteases – Destruction of enzymes released by neutrophils during inflammation – Ex: Elastase » Breaks down elastic fibers » Destructive process increases in people with low alpha1antitrypsin • Smoking – Increases # neutrophils in alveoli and release of elastase – Decreases effects of alpha1-antityrpsin • Break down of alveolar wall – – – – – Emphysema—Pathophysiology: Effects of Tissue Changes on Lung Function Decrease SA for gas exchange Loss of pulmonary capillaries Loss of elastic fibers Altered ventialtion-perfusion ratio Decreased support for small bronchi • Fibrosis and thickening of bronchial wall • Progressive difficulty with expiration – Air trapping, increased residual volume – Overinflation of lungs – Fixation of ribs in inspiration position Severe Emphysema • • • • Adjacent damaged alveoli Lung appears full of holes Frequent infection Lg. belbs near lung surface – May rupture • Pneumothorax • Pulmonary hypertension or R CHF Emphysema—Etiology • • • • Cigarette smokers Genetic Exposure to air pollutants Conjunction with other chronic lung disorders – Cystic fibrosis – Chronic bronchitis Emphysema—Signs and Symptoms • Onset insidious • Dyspnea occurs 1st on exertion • Hyperventilation with prolonged expiration – Use of accessory muscles, hyperinflation – ―barrel chest‖ • Anorexia, fatigue • Clubbed fingers Emphysema—Diagonstic Tests • Chest X-rays • Pulmonary function tests – Indicate presence of increased residual volume and total lung capacity – Decreased forced expiration volume and vital capacity Emphysema—Treatment • • • • • • Avoid resp infections, irritants Stop smoking Pulmonary rehabilitation Appropriate breathing techniques Maintain adequate nutrition, hydration Bronchodilators, antibiotics, oxygen therapy – As condition advances • Lung reduction surgery – Remove part of lung Chronic Bronchitis— Pathophysiology • Significant changes in bronchi – Irreversible and progressive • Inflammation, obstruction, repeated infection, chronic coughing • Inflamed, swollen mucosa • Hypertrophy/plasia of mucus glands – Increased secretions (increased # goblet cells) – Decreased ciliated epithelia • Fibrosis and thickening of bronchial wall – Further obstruction; pooling of secretions • Decreased oxygen – Cyanosis during cough • Severe dyspnea and fatigue • Pulmonary hypertension and R CHF Chronic Bronchitis—Etiology • Smoking – Crap! Not again! • Living in urban areas • Living in industrial areas Chronic Bronchitis—Signs and Symptoms • • • • • Constant productive cough Tachypnea, shortness of breath Thick, purulent secretions Severe cough and rhonchi Airway obstruction – Hypoxia, cyanosis • R CHF, pulmonary hypertension Chronic Bronchitis—Treatment • Decrease exposure to irritants • Expectorants, bronchodilators, chest therapy (postural drainage) – Remove excess drainage