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Name:_________________________________________ General Medicine Respiratory Disorders Lecture Notes Learning Objectives: Identify common manifestation of respiratory diseases: like Pneumonias, bronchopneumonia, bronchial Asthma. -Describe their classification, aetiology, clinical manifestations, investigations & treatment. - List the causes of dysnea, acute chest pain & haemoptysis Dr. J. Satish Kumar, MD, Department of Basic & Medical Sciences, AUST 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 Components of the Respiratory System Figure 23–1 Diagnostic Tests • • • • • • • Spirometry Arterial blood gas determination Oximeters Exercise tolerance Radiography Bronchoscopy Culture sensitivity tests General Manifestations of Respiratory Disease • Coughing – Irritation – Controlled by medulla – Constant, dry unproductive vs. productive cough • Sputum – – – – Mucus discharge Yellowish-green Rusty, dark-colored Thick, sticky • Hemoptysis • Dyspnea • Chest Pain 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 • • • • • • 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 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 Alveolar Organization Figure 23–11 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 Emphysema—Pathophysiology: Effects of Tissue Changes on Lung Function • Break down of alveolar wall – – – – – 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 COPDEmphysema 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 • 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 Dental Treatment Considerations for Asthmatics - avoid known triggers (stress, allergens, chemical irritants) - advise patient to continue taking usual medications - advise patient to bring inhalers to appointment - avoid elective treatments during upper respiratory infections when symptoms are poorly controlled - avoid use of aspirin and NSAIDS - watch sulfiting agents in LA with vasoconstrictor = bronchoconstriction - avoid erythromycin with theophylline = toxicity reaction - supplemental adrenal therapy with extreme stress in long-term steroid users Dental Treatment Considerations for Patients with COPD - promote smoking cessation - watch for wheezing, orthopnea while recumbent - activate EMS for acute respiratory distress - avoid sedatives - if severe COPD, risk for developing pulmonary hypertension, increasing risk for cardiac arrhythmias = avoid stress - adrenal supplementation may be necessary for patients taking long term steroids if procedure is likely to produce severe stress - oxygen (versus CO2) becomes drive for ventilation: if given too much oxygen, may induce apnea/acute respiratory failure - limit oxygen to less than 3L/minute, or deliver by nasal cannula during stressful/painful dental procedures - promote vaccination against influenza