The Respiratory System Lecture PDF

The Respiratory System Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com. Learning Objectives Explain the basic anatomic and physiologic principles of ventilation and gas exchange. 2. Describe the physiologic basis and use of pulmonary function te...

The Respiratory System Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com. Learning Objectives Explain the basic anatomic and physiologic principles of ventilation and gas exchange. 2. Describe the physiologic basis and use of pulmonary function tests. 3. Describe the causes, clinical effects, complications, and treatment of pneumothorax and atelectasis. 4. Describe the clinical symptoms, complications, and treatment of pneumonia. 5. Describe the histologic characteristics of a tuberculous infection. Explain the possible outcome of an infection. Describe the methods of diagnosis and treatment. 6. Differentiate between bronchitis and bronchiectasis. 7. List the anatomic and physiologic derangements in chronic obstructive lung disease. Explain its pathogenesis. Describe the clinical manifestations and methods of treatment. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com 1. Learning Objectives Describe the pathogenesis and manifestations of bronchial asthma and respiratory distress syndrome. 9. Explain the causes and effects of pulmonary fibrosis. Describe the special problems associated with asbestosis. 10. List the major types of lung carcinoma. Describe the clinical manifestations of lung carcinoma, and explain the principles of treatment. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com 8. Oxygen Delivery: A Cooperative Effort Circulatory system transports gases in the bloodstream https://en.wikipedia.org/wiki/Respiratory_system Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Respiratory system oxygenates blood and removes carbon dioxide ▪3 right (larger), 2 left lobes Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪Lung divided into lobes consisting of smaller units or lobules Lung: Structure and Function Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com System of tubes conduct air into and out of the lungs ▪ Bronchi: Largest conducting tube ▪ Bronchioles: Less than 1 mm ▪ Terminal bronchioles ▪ Respiratory bronchioles: Distal to terminal bronchiole with alveoli projecting from walls ▪ Alveoli: O2 and CO2 exchange (type I pneumocytes) have cells that produce surfactant (type II pneumocytes) Lung: Structure and Function Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com FIGURE 15-2 (A) Structure of a respiratory unit. Representative terminal bronchiole are designated TB. Respiratory bronchiole (RB) has alveolar sacs projecting from the wall of the bronchiole. Alveolar ducts are designated AD, and alveolar sacs are designated AS. Multiple alveoli (not labelled) open into each alveolar sac. Lung: Structure and Function Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com FIGURE 15-2 (B) Structure of terminal air passages. The interior of one alveolar duct is illustrated in cutaway view. Lung: Structure and Function (C) Courtesy of Leonard V. Crowley, MD, Century College. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com FIGURE 15-2 (C) Histologic structure of the lung illustrating alveoli and thin alveolar septa containing pulmonary capillaries (original magnification ×100). Gas Exchange Acinus or respiratory unit: Functional unit of lung (alveoli) Gas exchange occurs between alveolar air and pulmonary capillaries ▪ Atmospheric pressure at sea level is 760 mm Hg ▪ Partial pressure: Part of total atmospheric pressure exerted by a gas ▪ Partial pressure of oxygen (PO2) ▪ = 0.20 x 760 mm Hg = 152 mm Hg Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Respiration: Ventilation: Movement of air into and out of lungs (inspiration and expiration, respectively) Inspiration: caused by action of diaphragm (descends) and intercostal muscles (expand) Gas Exchange Alveolar air ▪ ↑ PO2 105 mm Hg ▪ ↓ PCO2 35 mm Hg Blood (pulmonary capillaries) PO2 20 mm Hg PCO2 60 mm Hg Requirements for efficient gas exchange (diffusion across alveolar membrane) ▪ Changes in atmospheric O2, CO2 ▪ Large capillary surface area in contact with alveolar membrane ▪ Unimpeded diffusion across alveolar membrane ▪ Normal pulmonary blood flow ▪ Normal pulmonary alveoli Impairment of any will result in impaired gas exchange Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Gases diffuse among blood, tissues and pulmonary alveoli due to differences in their partial pressures (occurs in reverse in tissues) The Pleural Cavity Pleural cavity: Potential space between lungs and chest wall Intrapleural pressure: Pressure within pleural cavity ▪ Normally less than intrapulmonary pressure ▪ Referred to as negative pressure or subatmospheric pressure because it is less than atmospheric pressure ▪ Tendency of stretched lung to pull away from chest creates a vacuum – aided by pleural fluid ▪ Release of vacuum in pleural space leads to lung collapse (loss of –ve pressure) ▪ Fluid (inflammatory or hemothorax) or air accumulation (pneumothorax) in pleural space can impair lung function Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Pleura: Thin membrane covering lungs (visceral pleura) and internal surface of the chest wall (parietal pleura) Pulmonary Function Tests ▪ Levels of arterial PO2 and PCO2 - monitored in COPD ▪ Pulse oximeter – measures oxygen saturation in blood Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Evaluate efficiency of pulmonary ventilation and pulmonary gas exchange ▪ Tested by measuring volume of air that can be moved into and out of lungs under normal conditions ▪ Vital capacity: Maximum volume of air expelled after maximum inspiration – can be used to evaluate progress of chronic disease (emphysema) ▪ One-second forced expiratory volume (FEV1): Maximum volume of air expelled in 1 second – can be used to detect airway narrowing in inflammatory or bronchospasm (Asthma) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Pneumothorax Escape of air into pleural space due to lung injury or disease Lung disease/damage increases susceptibility Spontaneous pneumothorax: No apparent cause Manifestations ▪ Chest pain ▪ Shortness of breath ▪ Reduced breath sounds on affected side ▪ Chest X-ray: Lung collapse and air in pleural cavity Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Stab wound or penetrating injury to chest wall: Atmospheric air enters pleural space Pneumothorax Chest tube inserted into pleural cavity; left in place until tear in lung heals ▪ Prevents accumulation of air in pleural cavity ▪ Aids re-expansion of lung Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Tension pneumothorax ▪ Positive pressure develops in pleural cavity ▪ Air flows through perforation into pleural cavity on inspiration but cannot escape on expiration ▪ Pressure builds up in pleural cavity, displacing heart and mediastinal structures away from affected side Atelectasis Collapse of lung (2 main causes) Compression atelectasis ▪ From external compression of lung by fluid, Air or Blood in pleural cavity ▪ Reduced lung volume and expansion Can also be caused as a response to pain (post operative) – patient does not breathe deeply or cough due to pain (splinting) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Obstructive atelectasis caused by bronchial obstruction from: ▪ Thick mucus secretions, tumor, foreign object ▪ Part of lung supplied by obstructed bronchus collapses as air is absorbed ▪ Reduced volume of affected pleural cavity ▪ Mediastinal structures shift toward side of atelectasis ▪ Diaphragm elevates on affected side FIGURE 15-9 (A) Chest x-ray before development of atelectasis. (B) Atelectasis of entire left lung. The collapsed lung appears dense because the air has been absorbed. The left half of the diaphragm is elevated. Trachea and mediastinal structures are shifted toward the side of the collapse. Courtesy of Leonard V. Crowley, MD, Century College. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Complete Atelectasis of the Left Lung Caused by Obstruction of Left, Main Bronchus Pneumonia Classification ▪ By etiology ▪ By anatomic distribution of inflammatory process ▪ By predisposing factors Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Inflammation of the lung ▪ Exudate spreads through lung ▪ Exudate fills alveoli ▪ Affected lung portion becomes relatively solid (consolidation) ▪ Exudate may reach pleural surface, causing irritation and inflammation Pneumonia Anatomic distribution of inflammatory process ▪ Lobar: Infection of one or more lobes of lung from bacterial pnemonia ▪ Bronchopneumonia: Infection of parts of lobes or lobules adjacent to bronchi by pathogenic bacteria ▪ Interstitial or primary atypical pneumonia: Caused by virus or Mycoplasma -involves alveolar septa rather than alveoli; septa with infiltrating lymphocytes, monocytes and plasma cells Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Etiology: Most important, serves as a guide for treatment ▪ Bacteria, viruses, fungi, Chlamydia, Mycoplasma, Rickettsia ▪ Most commonly – Streptococcus pneumoniae infection, risk of death in elderly Pneumonia Clinical features of pneumonia ▪ Fever, cough, purulent sputum, pain on respiration (if pleura involved), shortness of breath, impaired blood oxygenation ▪ Lung consolidation ▪ Elevated WBC Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Characterization by predisposing factors ▪ Any condition associated with poor lung ventilation and retention of bronchial secretions ▪ Post-op pneumonia: Accumulation of mucus secretions in bronchi ▪ Aspiration pneumonia: irritating substance, foreign body, food, vomit, water inhaled ▪ Obstructive pneumonia: Distal to bronchial narrowing Severe Acute Respiratory Syndrome (SARS) Manifestations ▪ Fever, chills ▪ Mild respiratory infection ▪ Occasional diarrhea ▪ Acute respiratory distress 3–7 days from onset: Cough, shortness of breath, evidence of pneumonia on X-ray; possibly requiring mechanical ventilation Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Highly communicable pulmonary infection ▪ Cause: Unusual coronavirus first identified in late 2002, last in 2004 ▪ 8422 cases with 11% fatality rate ▪ No effective antiviral therapy available against SARS ▪ SARS-associated virus not closely related to other coronaviruses ▪ Causes lower respiratory infections Middle Eastern Respiratory Syndrome (MERS-CoV) Infections still occurring – relatively low numbers (2500 total as of Jan 2021 – only 45 cases in 2020) Similar symptoms to SARS, but much more deadly than SARS (35% fatality) Small, isolated outbreaks Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com First identified in 2012 COVID – 19 (SARS Cov2) Current pandemic – began 2019 in China Age group IFR 0–34 0.004% 35–44 0.068% Over 200 million cases confirmed, over 4 million deaths 45–54 0.23% Most (80%) develop mild symptoms, 5% critical and require ventilation support 55–64 0.75% 65–74 2.5% Pneumonia common in hospital admissions from COVID19 (76%) 75–84 8.5% 85 + 28.3% Serious infection resembles SARS, comparatively low infection fatality rate (1-2% overall) that increases dramatically with age, and predisposing health factors (Infection Fatality Rate – IFR) Cause of world wide lockdowns and massive societal/ financial impacts Stimulated worldwide scientific effort with unprecedented vaccine development - protective Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Genetically similar to SARS Cov1 (83%) with extensive protein homology Pneumocystis Pneumonia ▪Affects mainly immunocompromised persons (AIDS patients, patients receiving immunosuppressive drugs, premature infants) ▪Organisms attack and injure alveolar lining, leading to exudation of protein material into alveoli ▪Cysts contain sporozoites released from cysts that mature to form trophozoites; sporozoites appear as dark dots at the center of cyst on stained smears Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Cause: Pneumocystis jiroveci, protozoan parasite of low pathogenicity Pneumocystis Pneumonia Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪Thick mucous/sputum too thick to expel creates – non-productive cough, dyspnea, pulmonary consolidation ▪Significant oxygen deficiency, significant increased SOB with ambulation ▪Diagnosis made by lung biopsy, bronchoscopy, or from bronchial secretions Usual Interstitial Pneumonia (UIP) Marked by patchy collagen distribution, scarring and fibroblast proliferation Tends to be viral or genetic (autoimmune) in origin Slow, gradual progress over a period of years FIGURE 15-22 Usual interstitial pneumonia (UIP). There are areas of fibroblast proliferation (black arrow) and collagen deposition (red arrow). Many areas show mononuclear inflammatory cells. Courtesy of Department of Pathology and Laboratory Medicine University of North Carolina at Chapel Hill. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Some interstitial pneumonias are characterized by injury to connective tissue causing fibrosis Tuberculosis Infection from acid-fast bacterium, Mycobacterium tuberculosis ▪ Alveolar Macrophages attempt to engulf – are primary conduit of infection spread ▪ Transmission: Airborne droplets ▪ Granuloma: aggregation of immune cells with central necrosis, indicates development of cell-mediated immunity ▪ Multinucleated giant cells: Bacteria plus fused macrophages and periphery of lymphocytes and plasma cells ▪ Organisms lodge within pulmonary alveoli ▪ Granulomas are formed ▪ Spreads into kidneys, brain, bones, uterus, fallopian tubes, others Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Bacterium has a capsule composed of waxes and fatty substances; resistant to destruction Tuberculosis ▪ Macrophages engulf bacteria, but are difficult to destroy and the proliferate inside the macrophages ▪ Granulomas are formed as immune cells (cellular immunity) attack TB and destroy some organisms ▪ In majority of cases (90%) – infection is arrested and granulomas in lung and regional LN scar over (latent TB) ▪ 10% of cases progress to primary TB or Infection may be reactivated: Healed granulomas contain viable organisms that are reactivated with reduced immunity (HIV/AIDS), leading to progressive pulmonary tuberculosis and extensive lung tissue damage ▪ Potential spreads through blood/lymph to other organs – kidney, bone, adrenal gland, uterus (extrapulmonary or secondary TB) ▪ Secondary focus of infection may progress, even if pulmonary infection has healed Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Caseous Granuloma – fibrous tissue surrounding central cluster of macrophages/giant cells, center region becomes necrotic as granulomatous inflammation progresses – highly characteristic of TB infection Miliary Tuberculosis Diagnosis ▪ Skin test, detects immune reaction to TB proteins (Mantoux test) – can detect latent ▪ Chest X-ray ▪ Sputum culture Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Miliary tuberculosis ▪ Systemic spread of TB (blood/lymph) ▪ Large numbers of organisms disseminated in body when a mass of tuberculous inflammatory tissue erodes into a large blood vessel ▪ Multiple granulomas (small, white nodules, 1–2 mm in diameter) of disseminated tuberculosis, enters multiple organs ▪ Extensive consolidation of one or more lobes of lung ▪ AIDS patients and immunocompromised individuals are at risk Drug-Resistant Tuberculosis Tx- combination drug regimen for several months (6-9 months) Resistant strains of organisms emerge with failure to complete treatment or premature cessation of treatment Multidrug-resistant tuberculosis (MDR TB) ▪ Tuberculosis caused by organisms resistant to at least two of the anti-tuberculosis drugs ▪ Course of treatment is prolonged ▪ Results less satisfactory Extensively drug-resistant tuberculosis (XDR TB) ▪ Caused by organisms no longer controlled by many antituberculosis drugs ▪ Found in eastern Europe, South Africa, Asia, some cases in the United States Newer 3HP (isoniazid/ rifapentine) treatments can reduce treatment to 3 months in latent TB – before progression Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Isoniazid, rifampin, ethambutol, pyrazinamide (first line tx) Bronchitis and Bronchiectasis Acute bronchitis: Inflammation of the tracheobronchial mucosa (sore throat common in URTI) Bronchiectasis: Walls thickened and weakened by chronic inflammation become saclike and fusiform ▪ Distended bronchi retain secretions ▪ Chronic cough; purulent sputum; repeated bouts of pulmonary infection ▪ Diagnosis made by bronchogram – air filled bronchi become visible by filling of alveolar space ▪ Bronchoscope – visualize airways for signs of damage/abnormalities, inflammation ▪ Exercise, oxygen therapy, drugs can provide symptom relief ▪ Only effective treatment is surgical resection of affected segments of lung Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Chronic bronchitis: From chronic irritation of respiratory mucosa by smoking or atmospheric pollution Chronic Obstructive Pulmonary Disease (COPD) Emphysema/Chronic bronchitis Chronic bronchitis: Chronic inflammation of terminal bronchioles; cough plus purulent sputum Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Pulmonary emphysema ▪ Destruction of fine alveolar structure of lungs with formation of large cystic spaces ▪ Destruction begins in upper lobes and eventually affects all lobes of both lungs ▪ Dyspnea initially on exertion; later, even at rest Chronic Obstructive Pulmonary Disease (COPD) Caused by chronic irritation: Smoking and inhalation of injurious agents Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Three main anatomic derangements in COPD 1. Inflammation and narrowing of terminal bronchioles ▪ Swelling of bronchial mucosa → reduced caliber of bronchi and bronchioles → increased bronchial secretions → increased resistance to airflow → air enters lungs more readily than it can be expelled → air trapped at expiration 2. Dilation and coalescence of pulmonary air spaces ▪ Diffusion of gases less efficient from large cystic spaces 3. Loss of lung elasticity; lungs no longer recoil normally following inspiration Chronic Obstructive Pulmonary Disease (COPD) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Pathogenesis ▪ Chronic Inflammatory swelling of mucosa ▪ Narrows bronchioles; increased resistance to expiration, causing air to be trapped in lung ▪ Leukocytes accumulate in bronchioles and alveoli, releasing proteolytic enzymes that attack elastic fibers of lung’s structural support ▪ Coughing and increased intrabronchial pressure convert alveoli into large, cystic air spaces; overdistended lung cannot expel air (air trapping) ▪ Retention of secretions predisposes to pulmonary infection and impairs gas exchange ▪ Increased susceptibility to respiratory infections Tx: Bronchodilators, inhaled steroids, oxygen therapy, lung therapy/exercise – lung transplant Chronic Obstructive Pulmonary Disease (COPD) Management ▪ Promote drainage of bronchial secretions to decrease frequency of pulmonary infections ▪ Oxygen therapy ▪ Bronchodilators, inhaled steroids ▪ Smoking cessation to halt damage progression ▪ Surgery does not improve survival; initial benefit is short term (lung volume reduction) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Lung damage caused by emphysema cannot be restored to normal Alpha1-Antitrypsin Deficiency Prone to emphysema development if levels are low (lower the level, higher the risk) ▪ Antitrypsin normally inactivates enzymes that may injure alveolar septa ▪ Susceptible to lung damage from smoking, atmospheric pollution, and respiratory infections Severe antitrypsin deficiency ▪ Digestion of connective tissues of alveolar septa, terminal air passages ▪ Develops progressive pulmonary emphysema ▪ Manifests in adolescence or early adulthood ▪ Tends to affect lower lobes of lungs ▪ Absent cough and excessive sputum production Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Antitrypsin: Alpha1 globulin; prevents lung damage from lysosomal enzymes (trypsin, fibrinolysin, thrombin) – produced by liver, monocytes ▪ Protects lungs from neutrophil “collateral damage” ▪ Concentration in blood under genetic influence ▪ Deficiency permits enzymes to damage lung tissue ▪ Autosomal dominant (1 mutation milder form of disease compared to double mutation) Bronchial Asthma Spasmodic contraction of smooth wall muscles of bronchi and bronchioles and increased bronchial mucous secretions in response to stimuli ▪ Can also be caused by stress, exercise, cold, smoke, pollutants, respiratory infection ▪ Dyspnea and wheezing on expiration (restricted air movement) ▪ Greater impact on expiration than on inspiration (leads to air trapping and over inflation) ▪ Spectrum disorder that depends on immune cytokines/ cell type involvement, mucosal repair/damage ▪ Child onset – typically allergic asthma Adult onset –occupational/environmental Treatment – identify/control triggers ▪ Fast acting bronchodilators (Ventolin), long-acting bronchodilators ▪ Long- acting drugs that reduce the reactivity of airways and block release of mediators from mast cells (Corticosteroids, anti-leukotrienes) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Attacks are often precipitated by allergens: Inhalation of dust, pollens, animal dander, other allergens (Atopy) – type 1 hypersensitivity Neonatal Respiratory Distress Syndrome Progressive respiratory distress soon after birth At-risk groups ▪ Premature infants ▪ Infants delivered by cesarean section ▪ Infants born to diabetic mothers Treatment ▪ Adrenal corticosteroids to mother before delivery ▪ Oxygen and surfactant (delivered by ET tube) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Pathogenesis: Inadequate surfactant in lungs ▪ Alveoli do not expand normally during inspiration ▪ Tends to collapse during expiration ▪ Increased permeability of pulmonary capillaries is increased (fluid rich in fibrinogen leaks into lungs) ▪ Compromised oxygen exchange Adult Respiratory Distress Syndrome Shock: Major manifestation – caused by damage to alveolar membrane and fluid leaking in Damaged alveolar capillaries leak fluid and protein Impaired surfactant production from damaged alveolar lining cells Formation of intra-alveolar hyaline membrane that blocks gas exchange Treatment – treat condition that caused shock (infection etc.), oxygen ventilator with slightly increased pressure (aids in diffusion) High mortality rate - 30-40% (COVID-19) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Conditions: Fall in blood pressure and reduced blood flow to lungs ▪ Severe injury (traumatic shock) ▪ Systemic infection (septic shock) ▪ Aspiration of acid gastric contents – alveolar damage ▪ Inhalation of irritant or toxic gases ▪ Damage caused by SARS (inflammation) Pulmonary Fibrosis Pneumoconiosis: Lung injury from inhalation of injurious dust or other particulate material ▪ Silicosis (rock dust) and asbestosis (asbestos fibers) ▪ Asbestos fibers also cancer (mesothelioma) ▪ Cotton fibers, coal dust Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Fibrous thickening of alveolar septa from irritant gases, organic and inorganic particles, inflammation, repair post ARDS ▪ Makes lungs rigid, restricting normal respiratory excursions ▪ Diffusion of gases hampered due to increased alveolar thickness ▪ Causes progressive respiratory disability similar to emphysema Vaping (E-cigarette) Induced Lung Injury Acute severe respiratory distress after vaping: SOB, chest pain – in some cases leading to development of chronic lung disease Syndrome termed EVALI (E cigarette or Vaping Associated Lung Injury) Could be associated with vaporizing medium or irritants in the suspension fluid. Some cases have shown similar alveolar damage to ARDS (fibrin exudates, fibroblast proliferation and hyaline membrane formation) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Vaporizers used to aerosolize nicotine Lung Carcinoma Usually smoking-related neoplasm ▪ Mortality from lung cancer in women exceeds breast cancer (kills 140 000/year in US) ▪ Arises from mucosa of bronchi and bronchioles: bronchogenic carcinoma ▪ Rich lymphatic and vascular network in lungs facilitates metastasis - Brain Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Common malignant tumor in both men and women who smoke Lung Carcinoma Classification and Prognosis Treatment: ▪ Surgical resection or radiation and chemotherapy for small cell carcinoma and advanced tumors ▪ If specific mutations (biomarkers) found in tumor cells (ie. EGFR – epidermal growth factor, ALK – anaplastic lymphoma kinase PD1… ) then treatment with specific blocking agents can be used Prognosis ▪ Depends on staging, histology, age, health, biomarkers ▪ Generally poor due to early spread to distant sites Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Classification ▪ Squamous cell carcinoma: Very common ▪ Adenocarcinoma: Very common ▪ Large cell carcinoma: Large, bizarre epithelial cells ▪ Small cell carcinoma: Small, irregular dark cells with scanty cytoplasm resembling lymphocytes; very poor prognosis The Respiratory System Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com.