1. COPD v. Asthma
Matt Genther

2. COPD Chronic Obstructive Pulmonary Disease (COPD)
Chronic bronchitis and Emphysema
Two forms of COPD with specific pathologic lung changes
Progressive irreversible airflow limitation
Associated with abnormal inflammatory lung response (McCance & Huether, 2010)
Chronic obstructive pulmonary disease (COPD) is a term to describe pathologic lung changes either emphysema or chronic bronchitis. There are distinct differences between chronic bronchitis and emphysema, but both are not fully reversible and associated with airflow limitations. Progressive airflow limitations can be exacerbated by abnormal inflammatory responses when lungs are exposed to noxious particles or gases (McCance & Huether, 2010).

3. COPD Tobacco smoke is the most common cause of COPD
Other causes include
Air pollutants, genetic factors, respiratory infections and occupational exposures (Postma, et al., 2014).
COPD is the third leading cause of death in the United states
12-16 million Americans report to have been diagnosed (Kim & Criner, 2013)
Most common to report
Age 65+, current and former smokers, women, hx of asthma, people with low incomes and individuals with less than high school income (McCance and Huether, 2010)
The primary cause of COPD is cigarette smoking both active and passive. Other risks include occupational hazards, pollution, and a history of severe childhood respiratory infections. Gender differences show women smokers have an increased susceptibility (McCance & Huether, 2010)

4. COPD – Chronic Bronchitis
Defined as being associated with chronic cough and sputum production
At least 3 months per year for 2 consecutive years
With increased exacerbation rate and accelerated decrease in lung function (Kim & Criner, 2013)
Chronic Bronchitis (CB) primary risk factor is smoking (42%) but can be found in 4-22% of non-smokers (Kim & Criner, 2013)
Potential risk factors include inhalation of biomass fuels, dust, and chemical fumes.
CB in an inflammatory disease of the mucous membranes in the bronchi. There is a marked increase in the amount of sputum produced over long periods of time. Chronic inflammation and irritation leads to an increase in goblet epithelial cells and mucous hyperplasia, leading to more thick secretions in the lungs and an increased risk of infection. The airways narrow increasing resistance and air trapping, the airway becomes obstructed (Higginson, 2010).

5. COPD – Chronic Bronchitis
Epidemiology of CB, high prevalence of patients with COPD
14-76% of all patients with COPD
10 million people in the US
Majority between years of age (Kim & Criner, 2013)
Image (Buggy, 2007)
Though many diagnosed with COPD exhibit both characteristics (emphysema and CB) the prevalence of CB is very high in COPD, up to 76% of all patients. There is a varying definition of CB because some criteria includes bronchiectasis, which is characterized by chronic cough, recurrent infections and viscous sputum. The pathophysiology does separate the two, approximately 10 million Americans are affected by CB, the majority of which are between years of age. Almost 25% of patients are older than 65, 31% between years of age (Kim & Criner, 2010).

6. COPD – Chronic Bronchitis
Inspired irritants increase mucous and number of goblet cells in airway
Creating thicker secretions
Increased mucous promotes bacterial cell growth
Embedded secretions impair airway function
Bronchial walls become inflamed leading to wall narrowing and bronchospasm (McCance & Huether, 2010)
Initially only the large bronchi are affected though all airways are involved
Obstruction greater on expiration
Profusion mismatch traps gas in distal lungs
Decrease tidal volume, hypoventilation, and hypercapnia (McCance & Huether, 2010)
Goblet cell hyperplasia, found in CB, increase fluid secretion in the lungs, the increased sticky and thick fluid is increasingly difficult for the lungs to expectorate (Kim & Criner, 2013). The worsened airflow can cause an increase in bacterial formation leading to the inflammatory process in the lungs. Ciliary capabilities are impaired leading to edema, bronchospasm, and eventual permanent narrowing of the airways starting at the large bronchi. The effects are seen mostly in expiration causing mismatch of perfusion and ventilation, leading to hypoxia. Airways collapse before air can be moved out of the lungs despite increased work from complementary respiratory muscles (McCance & Huether, 2010).

7. COPD – Chronic Bronchitis
Clinical manifestations:
Decreased exercise tolerance, wheezing, shortness of breath
Productive cough, frequent pulmonary infections, and copious thick sputum production. (McCance & Huether, 2010)
Forced expiratory volume (FEV1) and forced vital capacity (FVC) are declined in CB
Image (Kim & Criner, 2013)
Increased production of inflammatory cells, viral/bacterial infections lead to increased mucus in the airway. Oxygen and other gases are trapped in the alveolar space. Acute bronchitis is most often caused by respiratory viruses, but in chronic bronchitis epithelial cells release inflammatory mediators in response to noxious stimuli. The gross hypoxia leads to productive cough, dyspnea, wheezing, fatigue and hypoxemia (Higginson 2010).

8. COPD – Chronic Bronchitis
Diagnosis is based on a history of symptoms, physical exam, chest radiography and blood gas analysis (McCance & Huether, 2010)
Prevention is the best treatment because damage is irreversible
Smoking cessation before the damage is great is a mainline defense
Decreases goblet cell hyperplasia (Kim & Criner, 2013)
Antibiotics, mucolytics, corticosteroids, oxygen therapy and bronchodilators are first line medications for CB
Reduction of exacerbations, increase lung function and decreasing the infectious and inflammatory response of the body are the mechanisms of treatment (Poole, Black & Cates, 2012)
Mucous metaplasia is the pathologic cause of CB. Hypersecretion by goblet cells decrease the lungs ability to remove mucous and can lead infections. The over production of mucous impair cilia, causes distal airway occlusion, ineffective cough, weakened muscles, air trapping and reduced expiratory flow (Kim & Criner, 2013). Diagnosis is done on the basis of historical symptoms, physical exam, chest radiography, pulmonary function test and blood gas analysis. Prevention is the best measure against CB, smoking cessation is the top choice to reduce the progression of the disease. Bronchodilators and expectorants are used to reduce cough and secretions, nutritional counselling, deep breathing exercises, and recognition of early signs and symptoms of infection is required. Antibiotics are used in the management of acute exacerbations (sputum color change, increase wheezing or fever). Oral steroids are used during acute exacerbations and are not suggested for long term use (McCance & Huether, 2010).

9. COPD Emphysema
Emphysema is characterized by destruction of alveolar walls and enlargement of gas exchange airways (acini)
Elastic recoil is lost due to aging
Most likely cause of emphysema before old age is secondary to smoking (McCance & Huether, 2010)
Lungs have an elastic recoil ability to spring back into shape after being stretched. The ability of the lungs help to expire air from the lungs during exhalation. Emphysema is abnormal permanent enlargement of alveoli, where the alveolar cells lose elasticity and integrity of the walls around them. The alveoli become overinflated and destroyed decreasing surface are in the lungs. Impaired gas exchange follows emphysema and is classified by the location of the damage (Higginson, 2010).

10. COPD – Emphysema
Three classifications of Emphysema: Panacinar, Parasceptal and Centroacinar.
Panacinar emphysema destroys entire alveolus uniformly, mostly found in lower lungs
Parasceptal emphysema involves alveolar ducts and sacs in the peripheral lung
Centroacinar emphysema starts in the bronchioles and spreads towards the periphery (Higginson, 2010)
The classification for emphysema is based on the location of the destruction of lung tissue. Centriacinar emphysema occurs in the bronchioles and alveolar duct, usually in the upper lobes of the lung. The alveolar sac remains intact and is most common in smokers with CB. Panacinar emphysema involves the entire acinus (bronchioles, alveolar ducts, and alveoli) of the lower lobes, more likely to occur in advanced age and those without alpha 1 antitrypsin (McCance & Huether, 2010).

11. COPD – Emphysema
1-2% of cases are due to a lack of alpha-1 antitrypsin, in which alveoli lose elasticity
More commonly, noxious stimuli inhalation leads to emphysema
Cigarette smoke is the most common causing inflammatory response
Neutrophils, macrophages and lymphocytes produce chemicals that decrease the elasticity in cells, creating fewer larger alveoli (Higginson, 2010)
Inhaled toxins and air pollutants also know to cause emphysema
Smoking is the most common cause and progressive force of emphysema. Rare cases of primary emphysema are caused by inheritance deficit of alpha-1 antitrypsin, an inhibitory agent that prevents destruction of elastic cells in the lungs. Secondary emphysema is caused by noxious stimuli, local inflammatory response of the lung activates neutrophils, macrophages, and lymphocytes produce elastase that destroy the cell walls of alveoli. The destroyed cell walls lose surface area, elasticity and capability to move air into the blood stream. Venitilation perfusion mismatch increases the level of carbon dioxide in the body leading to hypoxemia and vasoconstriction (Higginson, 2010).

12. COPD – Emphysema
Emphysema is a progressive non- reversible disease of the alveoli
Hypoxemia causes the lungs to go through pulmonary hypoxic vasoconstriction
The constriction leads to pulmonary hypertension and eventual right sided heart failure, cor pulmonale (Higginson, 2010)
Pulmonary function tests indicate an obstructive gas exchange during expiration and a markedly low FEV1 (forced expiratory volume) and in increase is FRC (functional residual capacity), RV (residual volume), and TLC (total lung capcity). The capillary membranes of the alveoli are damaged and have less diffusion capabilities. Radiographic tests show the diaphragm that appears to be flattened and distended lung fields. The course of the disease is prolonged, causing pulmonary hypertension and ultimate right side heart failure (McCance & Huether, 2010).

13. COPD – Emphysema Clinical manifestations:
Dyspnea upon exertion and at rest, some unproductive coughing, thin stature and prolonged expiration
Barrel chest, hyperresonant percussion, pursed lip breathing and tripod breathing positioning (McCance & Huether 2010)
Diagnosis is based on respiratory signs and symptoms
Pulmonary function test
Size and shape of chest, breathing pattern, shortness of breath, clubbing of fingers, auscultation and percussion
X-ray, CT scans, arterial blood gases and EKG (Bailey, 2012)
During the progression of emphysema, gradual damage to the alveoli cause shortness of breath. The weakened and ruptured alveoli do not have the same surface area or function, which lets less air into the blood stream. The once elastic alveoli in emphysema no longer release gases causing the air to be trapped, not allowing oxygen rich are to be inhaled. The progression of the disease is slow at first, shortness of breath could be noticed during activities, but as the disease continues shortness of breath is found a rest (Bailey, 2012)

14. COPD - Emphysema
Smoking cessation primary mechanism to stop damage of emphysema
Oxygen therapy, pulmonary rehab, bronchodilators, corticosteroids, and surgery used to treat disease
Disease is irreversible
Treatments used to reduce symptoms, dyspnea and hypoventilation
Management of exacerbations is the main form of treatment, much like in CB. Individuals often use oxygen therapy. Inhaled bronchodilators are delivered by either inhalers or nebulizers. Oral corticosteroids and antibiotics are used during signs and symptoms of infection. Smoking cessation should be the first step in the treatment of emphysema, although the damage is irreversible progression of the disease can be slowed or stopped. Pulmonary rehab, improved nutrition and breathing techniques can all help provide therapy for emphysema (McCance & Huether, 2010).

15. Asthma
Chronic disorder of the airway, involving interactions of airway obstruction, bronchial hyperresponsiveness and inflammation (McCance and Huether, 2010)
This heterogeneous syndrome affects 300 million individuals worldwide
Airways suffer from chronic inflammation and small bronchial diameter (Aguilar, Walgama & Ryan, 2014)
Asthma is a chronic disorder that decreases the ability of the lungs to move oxygen and other gases during asthma attacks. Many cells cause the inflammatory response including mast cells, eosinophils, neutrophils, T-lymphocytes, macrophages, and damaged epithelial cells (McCance & Huether, 2010)

16. Asthma
Asthma occurs at all ages, half of all cases are found in children
Familial disorder linking over 100 genes with susceptibility
Eosinophils, mast cells, leukotrienes, and bronchial hyperresponsiveness increase the production of IgE
IgE plays a role in hypersensitivity and allergic response (Aguilar, Walgama & Ryan, 2014)
Risk factors: family history, exposure to pollutants and smoking, respiratory viral infections, and obesity (McCance & Huether, 2010)
Prevention and treatment of allergic rhinitis may prevent asthma (McCance & Huether, 2010)
Asthma is not age specific, though half of all cases happen to children and another third before the age of 40. More than 22 million Americans and 300 million people world wide suffer from asthma. Mortality has degreased since 1995 in the U.S. but asthma continues to increase with the increase in BMI (McCance & Huether, 2010)

17. Asthma
Inflammation causes wheezing, breathlessness, chest tightness and coughing
Most often at night or early morning
Episodes are widespread in lungs, resolve either spontaneously or with treatment (Postma, et al., 2014)
Expiratory flow is decreased by airway obstruction causing air trapping
Decreased alveolar perfusion causes hypoxia and respiratory acidosis and can lead to respiratory failure (McCance & Huether, 2010)
The insides of the walls of airways become swollen and become very sensitive, reacting dramatically to allergens or other irritating agents. Bronchial diameter related airflow is decreased during attacks, causing chronic wheezing and shortness of breath. Bronchodilators are used to increase oxygen flow into and out of the lungs (Postma, et al., 2014)

18. Asthma Host factors Perinatal factors Childhood exposures
Male sex in childhood, female sex in adulthood
Family history of COPD
(Family) history of asthma
Family history asthma/atopy
Genetic constitution
Airway hyperresponsiveness
Atopy —
Low lung function
Overweight
Perinatal factors
Maternal smoking
Maternal diet
Mode of delivery
Childhood exposures
Viral respiratory infections
Respiratory tract infections
No breastfeeding
Microbial deprivation
Environmental tobacco smoke exposure
Indoor air pollution
Air pollution
Adult exposures
Occupational exposures
Cigarette smoking
Outdoor air pollution
Risk factors of asthma are not age related and are worsened by cigarette smoking but is not often caused by smoking. The genetic disorder causing asthma is linked to some 100 genes. Family history is a risk factor as well as exposure to allergens, urban residence, exposure to air pollutions and cigarette smoke, obesity, and respiratory infections (McCance & Huether, 2010).

19. Asthma Pulmonary function tests are normal in between exacerbations
During attacks chest constricts, expiratory wheeze is present, dyspnea, coughing, tachycardia, prolonged expiration, and tachypnea
Prolonged bronchospasm can lead to status asthmaticus
Acidosis can follow PACO2 rises and can cause sudden death (McCance & Huether, 2010)
Increased exposure to allergens increases the likelihood of asthma. Cellular inflammation resulting in hyperresponsiveness of airways combined with cellular irritation causes inflammatory mediators to release chemicals that lead to bronchospasm and dilation. The resulting inflammation produces bronchial smooth muscle spasm, vascular congestion, increase vascular permeability, edema and thickening of airway walls will cause obstruction. (McCance & Huether, 2010).

20. Asthma
Diagnosis based on attacks, family history, allergies and an decreased FEV1, FVC and total lung capacity
Classified by severity: intermittent, mild persistent, moderate persistent and severe consistent (McCance & Huether, 2010)
Treatment includes avoiding allergens, short acting beta agonist inhalers for acute exacerbations, anti-inflammatory medications, and corticosteroids (Postma, et al., 2014)
Genetic and environmental factors contribute to the development of asthma and COPD. More severe airway hyperresponsiveness is found in the children of mothers that smoked during pregnancy, experienced higher air pollution and are more likely to become smokers themselves later in life. Abnormal lung development in utero, can cause underlying abnormal lung response that is expressed after inhalation of noxious chemicals that leads to inflammatory responses (Postma, et al., 2014).

21. COPD v. Asthma: Study Questions
Which form of emphysema damages the entire acinus and tends to not be associated with smoking?
Centriacinar emphysema
Panacinar emphysema
Paraseptal emphysema
Cor pulmonale
Which cells are NOT associated with inflammation and destruction of alveolar elasticity?
Neutrophils
Macrophages
Fibroblasts
Lymphocytes
Correct answers:
Which form of emphysema damages the entire acinus and tends to not be associated with smoking?
Centriacinar emphysema – highly associated with smoking
Panacinar emphysema – correct answer, damage is randomly throughout lung and is likely in elder populations and those with alpha-1 antitrypsin defeciency
Paraseptal emphysema – mostly alveolar sacs, associated with smoking
Cor pulmonale – considered right sided heart failure
Which cells are NOT associated with inflammation and destruction of alveolar elasticity?
Neutrophils – inflammatory cytokine
Macrophages – inflammatory cytokine
Fibroblasts – correct answer, fibroblasts are not associated with the breakdown of alveolar walls
Lymphocytes – inflammatory cytokine

22. COPD v. Asthma: Study Questions
Increased mucous production found in CB is associated with?
Goblet cell hyperplasia
Inflammatory cytokines
Pneumonia
Hypoventilation
Which group has a decreased risk for asthma?
Children of parents that smoke
Children living in cities
Children with many allergies
Children that live in rural areas
Pulmonary hypertension causes?
Left sided heart failure
Right sided heart failure
Diabetes
Tuberculosis
Increased mucous production found in CB is associated with?
Goblet cell hyperplasia – correct answer goblet cells replace regular epithelial cells in CB and produce high amounts of thick sputum
Inflammatory cytokines – not associated with increased mucous
Pneumonia – not associated with mucous production in CB
Hypoventilation – not associated with mucous production in CB
Which group has a decreased risk for asthma?
Children of parents that smoke – increase likelihood for both asthma and COPD
Children living in cities – increased likelihood because of exposure to pollutants
Children with many allergies – increase likelihood to develop asthma
Children that live in rural areas – correct answer, children in rural areas are not as exposed to pollutants
Pulmonary hypertension causes?
Left sided heart failure – not associated with pulmonary hypertension
Right sided heart failure – correct answer referred to as cor polumale, is secondary to pulmonary artery hypertension and right ventricular enlargement
Diabetes – not associated with pulmonary hypertension
Tuberculosis - not associated with pulmonary hypertension

23. References
Aguilar, P., Walgama, E., & Ryan, M. (2014). Other asthma considerations. Otolaryngologic Clinics Of North America, 47(1), doi: /j.otc
Bailey, K. (2012). The Importance of the Assessment of Pulmonary Function in COPD. Medical Clinics Of North America, 96(4),
Buggey, T. (2007). Storyboard for Ivan's morning routine. Diagram. Journal of Positive Behavior Interventions, 9(3), 151. Retrieved December 14, 2007, from Academic Search Premier database
Hadjiliadis, D. (2011). Emphysema. Retrieved from
Hadjiliadis, D. (2011). Cor pulmonale. Retrieved from
Higginson, R. (2010). COPD: pathophysiology and treatment. Nurse Prescribing, 8(3),

24. References
Kim, V., & Criner, G. (2013). Chronic bronchitis and chronic obstructive pulmonary disease. American Journal Of Respiratory & Critical Care Medicine, 187(3), doi: /rccm CI
McCance, K., & Huether, S. (2010). Alterations of Pulmonary Function. In Pathophysiology: The biologic basis for disease in adults and children (6th ed., pp ). Maryland Heights, Mo.: Mosby Elsevier
Poole, P., Black, P., & Cates, C. (2012). Mucolytic agents for chronic bronchitis or chronic obstructive pulmonary disease. Cochrane Database Of Systematic Reviews, (8), doi: / CD pub2
Postma, D., Reddel, H., ten Hacken, N., & van den Berge, M. (2014). Asthma and chronic obstructive pulmonary disease: similarities and differences. Clinics In Chest Medicine, 35(1), doi: /j.ccm