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1. Name of Student :

2. 2 Objectives Overview Obstructive Pulmonary Disorders OBSTRUCTION FROM CONDITIONS IN THE WALL OF THE LUMEN Asthma Acute Bronchitis Chronic Bronchitis OBSTRUCTION RELATED TO LOSS OF LUNG PARENCHYMA Emphysema OBSTRUCTION OF THE AIRWAY LUMEN Bronchiectasis Bronchiolitis Cystic Fibrosis Acute Tracheobronchial Obstruction Epiglottitis Croup Syndrome

3. OBSTRUCTIVE PULMONARY DISORDERS 3

4. Overview Obstructive lung diseases are manifested by increased resistance to airflow. Obstructive diseases of the lung can be classified into those involving 1.obstruction from conditions in the wall of the lumen (e.g., asthma, bronchitis) 2.obstruction resulting from increasing pressure around the outside of the airway lumen (e.g., emphysema secondary to loss of lung tissue and elasticity, enlarged lymph node, or tumor) 3.obstruction of the airway lumen (e.g., presence of a foreign body, excessive secretions, aspiration of fluids). These classifications are mainly terms of convenience because many respiratory disease processes involve several areas of the pulmonary system. Involvement of the airways produces narrowing of the passages so that airflow obstruction occurs. The major obstructive airway diseases are asthma, bronchitis, and emphysema. OBSTRUCTIVE PULMONARY DISORDERS 4

5. OBSTRUCTION FROM CONDITIONS IN THE WALL OF THE LUMEN Asthma Etiology: Asthma is a lung disease characterized by (a) airway obstruction that is reversible (but not completely in some patients), (b) airway inflammation, and (c) increased airway reactivity to a variety of stimuli. Airway inflammation leads to epithelial denudation, collagen deposition beneath the basement membrane, mast cell activation, mucosal edema, increased viscid secretions, and smooth muscle contraction. The immunohistopathologic features of asthma include denudation of airway epithelium, collagen deposition beneath the basement membrane, edema, mast cell activation, and inflammatory cell infiltration by neutrophils, eosinophils, and lymphocytes. Inflammation of the airway contributes to acute bronchospasm (bronchoconstriction), mucosal edema, mucous plug formation, and airway wall remodeling. Pathogenesis: 5

6. Asthma 6

7. Asthma (cont.) Wheezing feelings of tightness of the chest dyspnea cough increased sputum production Clinical manifestation: Diagnosis: The diagnosis of asthma is based on history, physical findings, sputum examination, pulmonary function tests, blood gas analysis, and chest radiography. Pharmacologic therapy for all three major obstructive disorders is similar and focuses on decreasing inflammation and broncho constriction, including β 2 agonists, corticosteroids, leukotriene modifiers, and mastcell inhibitors. Patients should be advised to avoid the objects in the environment thattrigger asthma attacks. Treatment: 7

8. Acute Bronchitis: Etiology: Acute inflammation of the trachea and bronchi is produced most by a variety of viruses such as influenza virus A or B, parainfluenza virus, respiratory syncytial virus, coronavirus, rhinovirus, Coxsackievirus, and adenovirus. Nonviral causes include Streptococcus pneumoniae, Haemophiles influenzae, mycoplasma, Moraxella, and Chlamydia pneumoniae. Pathogenesis: The airways become inflamed and narrowed from capillary dilation, swelling from exudation of fluid, infiltration with inflammatory cells, increased mucus production, loss of ciliary function, and loss of portions of the ciliated epithelium. Clinical Manifestation: Cough may be productive or non-productive low- grade fever Substernal chest discomfort sore throat postnasal drip fatigue 8

9. Acute Bronchitis (cont.) Diagnosis: Diagnosis of acute bronchitis is usually based on the clinical presentation, with recent onset of cough being the distinctive hallmark Treatment: Acute bronchitis is predominantly caused by viruses Viral infections do not respond to antimicrobial therapy Acute bronchitis caused by bacterial organisms responds well to antibiotic therapy. The primary goal in management is symptom management with antitussive agents,beta- 2 agonists, and other classes of bronchodilators in selective patients. Nonpharmacologic: recommendations are to increase fluid intake, avoid smoke, and use a vaporizer in the bedroom. 9

10. Chronic Bronchitis: Etiology: The major causes of chronic bronchitis are cigarette smoking repeated airway infections, genetic predisposition, and inhalation of physical or chemical irritants. Pathogenesis: Pathologic changes in the airway include chronic inflammation and swelling of the bronchial mucosa resulting in scarring, increased fibrosis of the mucous membrane, hyperplasia of bronchial mucous glands and goblet cells, hypertrophy of bronchial glands and goblet cells, and increased bronchial wall thickness, which potentiates obstruction to airflow.

11. Chronic Bronchitis (cont.) Clinical manifestation: Shortness of breath on exertion excessive amounts of sputum chronic cough excess body fluids (edema, hypervolemia), Chills malaise muscle aches fatigue loss of libido Insomnia. By the time dyspnea on exertion is present In the end- stage disease process, the patient presents with signs of right-sided heart failure (distended neck veins, right ventricular heave,right ventricular gallop, and peripheral edema). Hypoxia leads to pulmonary hypertension. Cyanosis is a late sign

12. Chronic Bronchitis (cont.) Diagnosis: Measures used to confirm the diagnosis include chest radiography, congested lung fields, an enlarged horizontal cardiac silhouette, and evidence of previous pulmonary infection. Arterial blood gas (ABG)↑ PaCO2,↓ Pao2 (often below 65 mm Hg); abnormal ABGs develop early in the disease process. The electrocardiogram may reveal atrial dysrhythmias and evidence of right ventricular hypertrophy. Secondary polycythemia related to continuous or nocturnal hypoxemia is common. Treatment: Pharmacologic treatment involves the use of inhaled short- acting β2 agonists and inhaled anticholinergic bronchodilators, cough suppressants antimicrobial agents for infections. Inhaled or oral corticosteroids may also be used in the treatment of some patients for acute exacerbations.

13. OBSTRUCTION RELATED TO LOSS OF LUNG PARENCHYMA Emphysema Emphysema Etiology: Emphysema (also referred to as type A COPD) is defined pathologically by destructive changes of the alveolar walls and abnormal enlargement of the distal air sacs. Smoking is commonly associated with emphysema Pathogenesis: The pathologic changes leading to alveolar destruction are associated with the release of proteolytic enzymes from inflammatory cells such as neutrophils and macrophages 13

14. Emphysema (cont.) Clinical manifestation: Cough difficulty in breathing progressive dyspnea Increasing shortness of breath Digital clubbing 14

15. Emphysema (cont.) Diagnosis : The diagnosis of emphysema is based on the patient’s history and physicalfindings, pulmonary function tests, chest radiographs, ABGs, andelectrocardiogram. Treatment: Poor prognosis is associated with weight loss, so treatment is focused on maintaining proper nutrition. Pharmacologic treatment involves the use of inhaled short- acting β2 agonists and inhaled anticholinergic bronchodilators, cough suppressants, and antimicrobial agents for infections. Inhaled or oral corticosteroids may also be used in the treatment of some patients for acute exacerbations. 15

16. OBSTRUCTION OF THE AIRWAY LUMEN • Bronchiectasis shape: saccular (with cavity- like dilatations) or cylindrical and with widening of the bronchial walls. A fusiform shape is a combination of saccular and cylindrical changes. Bronchiectasis Etiology: Bronchiectasis means dilation of bronchi. It is either acquired or congenital and is classified as both an obstructive and a suppurative(pus-forming) disorder. bronchiectasis can be classified according to bronchial Pathogenesis: Bronchiectasis is characterized by recurrent infection and inflammation of bronchial walls, which leads to persistent dilatation of the medium sized bronchi and bronchioles. H. influenzae is the most common cause of bacterial infections .

17. Bronchiectasis

18. Bronchiectasis (cont.) Clinical manifestation: Use of accessory muscles to breathe Pursed- lip breathing Minimal or absent cough Leaning forward to breathe Barrel chest Digital clubbing Dyspnea on exertion Diagnosis : The diagnosis of bronchiectasis is based on a history of chronic productive cough. The patient complains about producing copious amounts of foul- smelling, purulent sputum. Radiographic abnormalities may reveal small cysts, thickening of bronchial walls, and increased bronchial markings Treatment: Antibiotic therapy accompanied by inhalation of bronchodilators followed by vigorous chest percussion and postural drainage is the mainstay of treatment. 18

19. Bronchiectasis

20. Bronchiolitis Etiology: Bronchiolitis is characterized by widespread inflammation of bronchioles attributable to infectious agents such as respiratory syncytial virus(RSV) (50% of cases), influenza virus (type A, B, or C), or bacteria (H. influenzae, pneumococci, or hemolytic streptococci) and occasionally is produced by allergic reactions. Pathogenesis: Once initiated by the causal agent, proliferation and necrosis of bronchiolar epithelium occur, producing obstruction and increased mucus production

21. Bronchiolitis (cont.) Clinical manifestation: wheezing attributable to bronchospasm crackles decreased breath sounds retractions Increased sputum Dyspnea tachypnea (rapid, shallow respirations) low- grade fever Diagnosis: Patients commonly have an elevated WBC count. The chest radiograph may show enlarged air sacs, interstitial infiltrates, atelectasis, or severe hyperinflation. Treatment: Adequate oxygenation is maintained by providing humidified oxygen; monitoring blood gases or oxygen saturation; and administering oral, inhaled, or intravenous bronchodilator agents and, in selected cases, corticosteroids.

22. Cystic Fibrosis Etiology: Cystic fibrosis (mucoviscidosis) is an autosomal-recessive disorder of the exocrine glands. Cystic fibrosis can be classified either as an airflow obstructive disorder or as a suppurative (pus- forming) disorder. Hypersecretion of abnormal, thick mucus that obstructs exocrine glands and ducts isa characteristic finding in the disease. Pathogenesis: Cystic fibrosis is classified as an autosomal-recessive disorder. One genetic defect associated with cystic fibrosis involves deletion of three base pairs in codon 508 (AF508) that code for phenylalanine on chromosome 7 (band q31).This is the most common genetic mutation causing cystic fibrosis and occurs in 60% to 75% of cystic fibrosis patients tested. 22

23. Cystic Fibrosis (cont.) Clinical manifestation: history of cough in a young adult or child thick, tenacious sputum; recurrent pulmonary infections (commonly Pseudomonas aeruginosa) recurrent episodes of bronchitis. Diagnosis: The diagnosis of cystic fibrosis is based on clinical and laboratory findings.Diagnostic studies that are routinely performed include ABG measurements, pulmonary function tests, sputum culture and sensitivity with Gram stain, and chest radiography. Specific diagnostic tests for cystic fibrosis include stool examination for fat, pilocarpine iontophoresis (sweat test), and genetic testing. Treatment: Treatment includes the use of bronchodilators, and mobilization of the thick mucus by postural drainage and chest physiotherapy (percussion and vibration) is a priority. Alternative methods for mucus removal include the forced expiratory technique, which involves coughing(huffing) with an open glottis. 23

24. Acute Tracheobronchial Obstruction 24 Etiology: Acute tracheobronchial obstruction requires immediate treatment. Causes frequently include aspiration of a foreign body, mispositioned endotracheal tube, laryngospasm,epiglottitis, trauma, swelling from smoke inhalation, postsurgical blood clot, and compression of the bronchus or trachea by tumors or enlarged lymph nodes. Pathogenesis: Obstruction by one of the etiologic agents can be partialor complete. The health care worker must be prepared to assess thesituation rapidly and act immediately to clear the airway

25. 25 Acute Tracheobronchial Obstruction (cont.) Clinical manifestation: inability to talk, tachycardia cyanosis rapid progression to unconsciousness unlessthe problem is quickly reversed Diagnosis: The diagnosis of airway obstruction is based on clinical features andABG analyses. ABG values frequently show hypoxemia and hypercarbia.Chest radiographs may reveal the location of the obstruction Treatment: Treatment involves opening the obstructed airway as quickly as possible.Blows to the patient’s back or use of abdominal thrusts (previouslycalled the Heimlich maneuver) may be necessary for the foreign body to be expelled.

26. •Epiglottitis Epiglottitis is a rapidly progressive cellulitis of the epiglottis and adjacent soft tissues. Acute epiglottitis is suspected when odynophagia (pain with swallowing) seems out of proportion to pharyngeal findings Etiology : Pathogenesis : The infecting agent localizes in the supraglottic area in the epiglottis and pharyngeal structures, causing rapid and potentially fatal inflammation with swelling and airway obstruction. Clinical manifestation : Drooling, Dysphagia, Rapid Onset of Fever Dysphonia Inspiratory Stridor Inspiratory Retractions Diagnosis : Definitive diagnosis is obtained by direct or fiberoptic visualization of the epiglottis. Treatment : Antibiotic therapy should be started immediately

27. • Etiology: Viral croup affects the larynx, trachea, and bronchi. It is often caused by parainfluenza virus type 1.Other potential infecting organisms include parainfluenza types 2 and3, RSV, influenza virus, adenovirus, and Mycoplasma pneumoniae. • Pathogenesis: The infectious agent causes inflammation along the entire airway, leading to edema formation in the subglottic area • Clinical Manifestation: Upper respiratory tract infection or cold that has developed into a barking cough with stridor. Fever is low grade or absent. • Diagnosis: Diagnosis is based on clinical manifestations and lateral neck films to rule out epiglottitis. Direct laryngoscopy is also used to confirm the presence of epiglottitis because the clinical presentation is similar to that of croup. • Treatment: Supportive treatment is used for viral croup. Mist therapy, oral hydration, and avoidance of stimulation are used in outpatient therapy. Croup Syndrome

28. • Obstructive pulmonary disorders are characterized by increased resistance to airflow. With bronchiectasis, obstruction is due to inflammation, infection, and dilatation of the bronchioles. • Similarly, bronchiolitis is associated with inflammation; inflammation leads to mucosal edema and excessive mucus production. Airway obstruction from cystic fibrosis is related to production of excessive, thick secretions. • • Obstruction of the airway in croup is the result of edema and increased secretions caused by viral infection. • Similarly, epiglottitis is an infectious process requiring emergency treatment. The inflammation is associated with increased mucus production and edema of the tracheal bronchial mucosa in asthma and bronchitis. Bronchospasm of the tracheobronchial tree attributable to exposure to allergens, pulmonary irritants, stress, and exercise may result in hypoxemia. Obstruction to airflow in emphysema is due to loss of alveoli and small airways. The most common cause is cigarette smoking. SUMMARY Obstructive pulmonary diseases include airway obstruction, obstruction from conditions affecting the tracheobronchial walls loss of lung parenchyma (emphysema).

29. Banasik, J. L. (2019). Pathophysiology. Elsevier Health Sciences. REFERENCE 29

30. Thank you 30