COPD

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What is the leading cause for the development of COPD?

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1

What is the leading cause for the development of COPD?

Cigarette smoking

  • 15-20% of smokers dx with COPD

  • 80-90% of those dx with COPD are smokers

  • Smoking is toxic to lung cells impairs the mechanisms responsible for lung repair

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2

What else can contribute to the development of COPD?

  • Genetics

  • Environment

  • Other risk factors

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3

How do genetics contribute to the development of COPD?

  • Polymorphisms of genes that code for TNF, surfactant, proteases and antiproteases

  • Inherited mutation in a-1 antitrypsin gene can cause early onset and severe COPD (onset and severity worsened by smoking)

  • Heterogeneous nature of COPD attributed to multiple genetic and environmental factors as well as gene-gene and gene-environment interactions (epigenetic's)

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4

How does environment contribute to the development of COPD?

Long term exposure to occupational dusts/chemicals, indoor pollution from heating and cooking with biomass fuels, outdoor pollution

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5

What are some other risk factors that can lead to the development of COPD?

  • Severe childhood respiratory infections

  • Asthma

  • Airway hyper-responsiveness

  • Impairment to fetal development resulting in low birth weight

  • Infants who develop bronchopulmonary dysplasia

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6

What is meant by the use of the term "COPD phenotypes"?

Not a single disorder, but a group of disorders that are characterized by airflow limitation

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7

What are the 3 COPD phenotypes?

  • Chronic bronchitis

  • Emphysema

  • Bronchiectasis

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8

What is chronic bronchitis?

  • Airway inflammation and obstruction of the major and small airways

  • Chronic productive cough for at least 3 consecutive months over 2 consecutive years

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9

What is emphysema?

  • Loss of lung elasticity

  • Abnormal enlargement of the airspaces distal to the terminal bronchioles with destruction of the alveolar walls and capillary beds

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10

What is bronchiectasis?

  • Permanent dilation of the bronchi and bronchioles

  • Caused by destruction of the muscles and elastic supporting tissue due to vicious cycles of infection and inflammation

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11

How are asthma and COPD related?

Together they can be called obstructive airway diseases

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12

How can COPD be defined?

"Respiratory disorder largely caused by smoking, characterized by progressive, partially reversible airway obstruction and lung hyperinflation, systemic manifestations and increasing frequency and severity of exacerbations"

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13

What is COPD characterized by?

  • Persistent inflammation of airways, lung parenchyma and its vasculature

  • Pathophysiological hallmark is expiratory flow limitation

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14

What are the 4 most important airflow limitation mechanisms associated with COPD?

  • Loss of lung elastic recoil

  • Peribronchiolar fibrosis

  • Increased airway secretions

  • Airway smooth muscle

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15

Describe what occurs with loss of lung elastic recoil

  • Occurs with emphysema

  • Due to protease mediated degradation of connective tissue elements in the lungs

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16

Describe what occurs with peribronchiolar fibrosis

  • Occurs because of imbalance between lung repair and defence mechanisms

  • Fibrosis of small airways contributes to airway remodelling which is a key factor in the development of the irreversible airflow limitation seen in COPD

  • Airway remodelling: "persistent changes that occur within the structural components of the airways in response to inflammation"

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17

Describe what occurs with increased airway secretions

  • Mucus hyperplasia and increased expression of mucin genes in COPD

  • Inflammation and oxidant injury play a role in mucus hypersecretion

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18

Describe what occurs to airway smooth muscle in COPD

  • Increased tone in airway smooth muscle due to bronchial hyper-reactivity and bronchoconstriction due to persistent inflammation

  • Even if tone is not increased in those with COPD, airways are narrower resulting in increased airway resistance

  • Using bronchodilators will have a positive effect on airflow whether there is increased tone or not

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19

Chronic bronchitis is the result of?

Inflammation of the airway epithelium and mucus hyper-secretion due to inspired irritants like tobacco smoke or air pollution

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20

What is the first feature of chronic bronchitis?

Hyper-secretion of mucus in the large airways

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21

What are some of the issues associated with increased mucus production and chronic bronchitis?

  • Mucus produced is thicker and more tenacious

  • Increase in the number and size of mucus glands and goblet cells in the airway epithelium

  • Ciliary function impaired which reduces airway clearance

  • increases risk of pulmonary infection because lung's defense mechanisms are compromised

  • Bacterial colonization can occur, infection and injury cause further mucus production and inflammation

  • Recurrent infections and persistent inflammation result in bronchospasm and eventually permanent narrowing of the airways

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22

How does thick mucus and hypertrophied bronchial smooth muscle lead to pulmonary HTN and cor pulmonale?

Thick mucus and hypertrophied bronchial smooth muscle -> airway obstruction -> ventilation-perfusion mismatch + hypoxemia + hypercapnia -> polycythemia, cyanosis -> pulmonary hypertension and cor pulmonale

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23

What is polycythemia?

Overproduction of red blood cells

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24

What is cor pulmonale?

Enlargement of the right ventricle which will cause right sided heart failure

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25

What is emphysema characterized by?

Breakdown of elastin in the alveolar septa and bronchial walls as well as breakdown of alveolar and bronchial wall components by proteases (enzymes that digest proteins)

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26

Why is there breakdown of lung tissues by proteases?

There is an imbalance between proteases and anti-proteases, the leading cause of this is airway epithelial inflammation from toxins in tobacco smoke or air pollution

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27

What are the most important proteases activated in emphysema?

  • Elastases

  • Cathepsins

  • Matrix malloprotease

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28

How is protease production and smoking linked?

Anti-protease production and release is inadequate in smokers that develop COPD

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29

What is primary emphysema?

Related to inherited linked deficiency of a-1 antitrypsin, individuals develop the disease before the age of 40/in their early 40's and do not have a history of smoking. People with the deficiency who also smoke have a higher susceptibility to developing emphysema

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30

What are some of the things that occur to someone with emphysema?

  • Septal destruction destroys portions of the pulmonary capillary bed which leads to ventilation-perfusion mismatch and hypoxemia

  • Decreased elastic recoil in bronchial walls leads to air trapping

  • Air trapping causes enlargement of gas exchange airways called acini

  • Increased residual volume and total lung capacity occur due to air trapping, persistent inflammation can also result in hyper-reactivity of the bronchi with bronchoconstriction

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31

What does a-1 antitrypsin do?

  • Elastin is released by inflammatory cells in response to smoking/air pollution. A-1 antitrypsin normally inhibits the action of elastin, however inflammation will persist and there is a decrease in a-1 antitrypsin activity

  • This leads to destruction of elastic fibres in the lung and causes emphysema

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32

What occurs with a-1 antitrypsin deficiency?

  • Limited amount of a-1 antitrypsin to counteract elastase released

  • Result is destruction of elastic fibres in the lung and eventual emphysema

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33

How is the amount of a-1 antitrypsin determined?

By protein inhibitor genes

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34

What is the most serious disorder of the a-1 antitrypsin deficiency?

Caused by the PIZ variant which is found in 5% of the population. Homozygous individuals who carry 2 PIZ genes have only 15-205 of the normal plasma [ ] of a-1 antitrypsin and have a 70-80% likelihood of developing emphysema

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35

What role do sites of involvement play in emphysema?

Determines whether the emphysema is centriacinar or panacinar

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36

What is the most common form of emphysema?

Centriacinar, destructions confined to terminal and respiratory bronchioles, located in the upper parts of the lungs

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37

What is paracinar emphysema?

Involves the peripheral alveoli and later the more central bronchioles, more common in those with inherited a-1 antitrypsin deficiency, located in the lower parts of the lungs

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38

When does air trapping occur?

  • Airways pulled open during inspiration allowing gas to flow past the obstruction caused by narrowed airways and mucus plugs

  • During expiration decreased elastic recoil of bronchial wall causes airways to collapse and prevents normal expiratory flow

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39

What would you expect to find upon physical examination of someone who has hyperinflation/air trapping of the lungs?

  • Barrel chest

  • Expands the thorax (respiratory muscles at mechanical disadvantage resulting in decreased tidal volume, hypoventilation and hypercapnia)

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40

Which condition is air trapping usually most associated with?

Usually associated more with emphysema as the loss of elastic recoil due to destruction of lung tissue significantly prevents normal expiratory flow

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41

How does inflammation relate to COPD?

  • Central feature of COPD

  • leads to damage and remodelling of lung parenchyma, leading to airflow limitation

  • Innate immunity activated at all stages of COPD, adaptive immunity is activated in more severe disease

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42

What changes would we expect to see in the lymphocytes of a person with COPD?

  • Increase in lymphocytes

  • Increase in CD4+ lymphocytes and B-cells

  • Macrophages secrete inflammatory mediators that activate neutrophils and CD*+ T-lymphocytes

  • CD4+ T-lymphocytes activate B-cells, and B-cells involved

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43

What are the most important inflammatory cells in COPD?

  • Neutrophils

  • Macrophages

  • CD8+ T-lymphocytes

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44

In a person with COPD, we could expect to see an increase in which pro-inflammatory cytokines?

  • TNF-a

  • IL-1B

  • IL-6

  • IL-32

  • Thymic stromal lymphopoietin

  • T-cell cytokines

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45

How do chemokines, growth factors and anti-inflammatory cytokines influence COPD?

  • Chemokines induce leukocyte chemotaxis, promote neutrophil activation and migration

  • Growth factors contribute to airway remodelling

  • Cytokines have inhibitory/anti-inflammatory effects

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46

What is IL-10? What happens to levels of this in patients with COPD?

  • Persistent anti-inflammatory cytokine that inhibits TNF-a, IL-1B, granulocyte-macrophage colony-stimulating factor, chemokines and matrix metalloproteinase (all increased in COPD)

  • IL-10 is reduced in the sputum of persons with COPD

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47

What are the 2 schools of thought in relation to systemic inflammation and COPD?

  1. Systemic manifestations and comorbidities are the result of a systemic spill over of the inflammatory and respiratory events occurring in the lungs. Therapies should be primarily directed to the lungs

  2. Pulmonary manifestations are simply one form of expression fo a systemic inflammatory state where there is multiple organ compromise. Therapies should be shifted to the systemic inflammatory state

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48

Where are most treatments for COPD currently aimed?

At the lungs

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49

What are the cytokines linked to muscle weakness, skeletal muscle atrophy or cachexia?

  • IL-6

  • TNF-a

  • IL-1B

  • Chemokines (specifically CXCL8 or IL-8)

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50

What is leptin?

  • Adipokine (cytokine derived from fat cells)

  • Important role in regulating energy and is decreased in persons with COPD

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51

What are the acute phase proteins linked to COPD symptoms and severity?

  • CRP - linked to health and exercise capacity, significant predictor of BMI, if it remains high 2 weeks post exacerbation there is a likelihood of recurrent exacerbation

  • Fibrinogen - plasma concentrations increased with frequency exacerbations, worse FEV1 and increased risk of hospitalization for COPD linked to increased plasma fibrinogen

  • Serum amyloid A - elevated during exacerbation correlated wit severity of exacerbations

  • Surfactant protein D (better related disease severity and symptoms than CRP

  • CRP and fibrinogen associated with increased cardiac co-morbidity

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52

What are the systemic manifestations (of inflammation) and comorbidities? (* = comorbidity, not usually related to systemic inflammation)

  • Skeletal muscle weakness

  • Cachexia

  • Lung cancer*

  • Pulmonary HTN*

  • Ischemic heart disease

  • Cardiac failure

  • Osteoporosis

  • Normocytic anemia

  • Diabetes

  • Obstructive sleep apnea*

  • Depression

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53

What is the role of oxidative stress from cigarette smoke?

  • Contains numerous oxidants as well as from inflammatory cells which release reactive oxygen species

  • Oxidant/antioxidant imbalance

  • Other factors affecting O/AO imbalance in pathogenesis of COPD are respiratory infections, genetic factors and dietary factors

  • Oxidative stress contributes to the damage that occurs in the lungs

  • Oxidative stress considered to be the cause of corticosteroid resistance in COPD

  • Muscle dysfunction in COPD strongly associated with enhanced oxidative stress

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54

Define AECOPD

Acute changes in symptoms such as cough, dyspnea and sputum production that is beyond what is considered normal variability in a patient

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55

Why is it difficult to determine which bacteria cause AECOPD?

Chronic bacterial colonization of the airways is common in COPD

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56

What are some triggers of AECOPD?

  • CHF

  • Pulmonary embolis

  • Exposure to allergens and irritants

  • Bacterial/viral infections

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57

What are the most frequently involved viruses in AECOPD?

  • Rhinoviruses

  • Respiratory syncytial virus (RSV)

  • Influenza

  • Coronaviruses

  • Parainfluenza viruses

  • Human metapneumoviruses

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58

What are some of the probable bacterial pathogens involved in COPD?

  • Haemophilus influenza

  • Moraxella catarrhalis

  • Streptococcus pneumonia

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59

Which type of infection more commonly causes AECOPD?

Viral more common than bacterial

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60

What are the common signs and symptoms of AECOPD?

  • Breathlessness

  • Wheezing

  • Chest tightness

  • Increased cough and sputum production

  • Change in colour and tenacity of sputum

  • Fever

  • Tachycardia

  • Tachypnea

  • Malaise

  • Insomnia

  • Fatigue

  • Depression

  • Confusion

  • Exercise intolerance and fever may present prior to exacerbation

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61

How can acute exacerbations be managed?

  • Initiate or increase bronchodilator therapy

  • No improvement -> admission to hospital

  • Administer oxygen, combination therapy of beta-2 agonists and anti-cholinergic, PO/IV corticosteroids

  • IV methylxanthines, antibiotics, NIPPV my be considered

  • Treat comorbidities prn

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62

How can acute exacerbations be prevented?

  • Smoking cessation

  • Vaccinations (specifically influenza which reduces mortality by 50% and pneumococcal vaccine)

  • Self management education

  • Regular long acting bronchodilators in moderate to severe COPD

  • Regular inhaled corticosteroid and long acting beta-2 agonist combination therapy in moderate to severe COPD with 1+ AECOPD per year

  • Oral corticosteroid therapy for AECOPD

  • Pulmonary rehabilitation

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63

What are some of the symptoms that those with COPD can experience?

  • Dyspnea/SOB

  • Fatigue and exercise intolerance

  • Cough

  • Sputum production

  • Wheezing

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64

Why would someone with COPD experience dyspnea/SOB?

Being unable to get enough air, dyspnea may be caused by disturbances in ventilation, gas exchange or ventilation-perfusion relationships, and increased work of breathing that damages the parenchyma

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65

Why would someone with COPD experience fatigue and exercise intolerance?

Breathing with effort depletes their energy stores

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66

Why would someone with COPD experience a cough?

Reflex stimulated by excessive secretions and/or inhaled irritants

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67

Why would someone with COPD experience sputum production?

Excessive amounts caused by airway inflammation

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68

Why would someone with COPD wheeze?

Breathing through narrowed airways

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69

What are some abnormal vital signs that you may expect to see in someone with COPD? What would each abnormality indicate?

FEVER - may indicate infection HYPOVENTILATION - due to prolonged expiratory phase TACHYCARDIA - related to mechanisms including fever, use of beta-2 agonist and hypovolemia BP - should not be affected, abnormal results may indicate hypovolemia or sepsis (hypotension), high blood pressure = HTN HYPOXEMIA - Inadequate gas exchange in COPD

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70

What are some cardiac abnormalities that you could expect to see in someone with COPD?

Edema or increased jugular venous pressure

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71

What are some respiratory abnormalities that you could expect to see in someone with COPD?

  • Most important assessment

  • Note work of breathing, use of accessory muscle, pursed lip breathing, cyanosis, hyper resonance with percussion, crackles, wheezes

  • Barrel chest

  • Tripod position to facilitate use of sternocleidomastoid, scalene and intercostal muscles

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72

What are some other signs (related to physical appearance) that you may expect to see in a patient with COPD?

  • Muscle weakness

  • Muscle wasting

  • Cachexia

  • Clubbing (associated with diseases that interfere with oxygen)

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73

Why do you hear hyper resonance when auscultating the chest of someone with COPD?

Due to air trapping in the lungs

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74

Why would you hear crackles when auscultating the chest of someone with COPD?

Abnormal secretions, mucus or fluid in the airways

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75

Wheezes on inspiration indicate...?

Upper airway obstruction

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76

Wheezes on expiration indicate...?

Lower airway obstruction

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77

What signs would we expect to see in arterial blood gas of someone with COPD?

  • Hypoxemia, hypercapnia, acidosis with severe disease or respiratory failure (inadequate gas exchange)

  • Hypoxemia in which pp or arterial 02 is less than or equal to 50 mmHg or hypercapnia where pp of arterial CO2 is greater than 500 mmHg with a pH less than or equal to 7.25

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78

What signs would we expect to see in a CBC of someone with COPD?

  • Elevated leukocytes

  • Anemia

  • Elevated cytokines and acute phase proteins

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79

What would you expect to see on a chest x-ray of someone with COPD?

  • Hyperinflation and flattening of the hemi-diaphragms (air trapping)

  • Note presence of atelectasis, pulmonary edema, areas of consolidation, cardiomegaly

  • Evidence of infection

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80

What is the standard assessment tool for diagnosis, staging and monitoring of COPD?

Spirometry

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81

When should spirometry be performed?

Anyone with a history of exposure to risk factors for COPD, history of chronic respiratory illness or chronic symptoms of cough, sputum production or dyspnea

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82

What is forced expiratory volume in 1 second (FEV1)?

Volume of air forcibly exhaled during the first second of expiration after maximal inspiration

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83

FEV1 <80% indicates what?

More advanced disease

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84

What is forced vital capacity?

Maximum volume of air exhaled until the lungs are empty

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85

How is FVC affected in COPD?

FVC not always reduced in the early stages of COPD

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86

What ratio is used to assess lung function?

Ratio of FEV1 to FVC

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87

What value confirms airflow limitation?

FEV1/FVC post bronchodilator value of < 0.70

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88

How is oxygen therapy used in the treatment of COPD?

  • Used during stage IV COPD, which is very severe disease with chronic respiratory failure

  • Long term continuous therapy, during exercise or prn to relieve episodes of acute dyspnea

  • LT therapy (15+ hours a day) to achieve 02 sats of 90%+ offers a survival advantage not those with stable COPD with severe hypoxemia (pp O2 mmHG or less/ pp O2 <60 mmHg in presence of bilateral ankle edema, cor pulmonale or hematocrit >56%)

  • Improves pulmonary HTN, increases exercise capacity, lung function, improves the mental and emotional states, and increases survival in persons with chronic respiratory failure

  • Noninvasive positive pressure ventilation can be considered during severe exacerbations or in persons with chronic hypercapnia respiratory failure, not standard for those with COPD

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89

What role do bronchodilators play in COPD?

Main pharmacological therapy for those with COPD, available in long acting and short acting formulas Ex. Inhaled anticholinergics, inhaled beta-2 adrenergic receptor agonists

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90

What do inhaled anticholinergics do?

  • Decrease bronchoconstriction by reducing muscle tone and glandular mucus

  • Inhibits acetylcholine from interacting with cholinergic M1 and M3 receptors that control bronchoconstriction and glands that produce mucus

  • Caution with glaucoma/prostate issues

  • Dry mouth = common side effect

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91

What do inhaled beta-2 adrenergic receptor agonists do?

  • Cause bronchodilation

  • Act on B2 adrenergic receptors located in smooth muscle of the airways

  • Receptors stimulated, causes increase in cAMP which inhibits bronchoconstriction

  • LABAs recommended as maintenance therapies for long term prevention and reduction of symptoms

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92

What are combination inhalations?

Combine inhaled anticholinergics or beta-2 adrenergic receptor agonists with corticosteroids

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93

Why are corticosteroids not effective as a mono therapy for those with COPD?

Because of corticosteroid resistance (oxidative and nutritive stress in COPD lungs)

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94

What are inhaled corticosteroids used for in those with COPD?

  • Treatment of patients with advanced COPD (FEV1 <50% with frequent exacerbations)

  • ICS + LABA reduce decline in lung function

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95

What are oral corticosteroids used for in those with COPD?

Used for severe exacerbations

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96

What are some other forms of pharmacotherapy that can be used for the management of COPD?

  • Methylxnthines - 3rd line treatment after inhaled anticholinergics or inhaled beta-2 agonists or when treating exacerbations

  • Mucolytics can be used in patients with significant mucus hyper secretion

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97

Rehab should be offered and encouraged to who?

  • People with COPD need to maintain an active lifestyle

  • Rehab should be offered and encouraged for those who continue to have dyspnea and exercise limitation despite optimal pharmacotherapy

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98

What benefits does physical therapy provide?

  • Reduces symptoms, improves dyspnea, exercise endurance and quality of life

  • Increases physical and emotional participation in ADL

  • Decreases risk of hospitalization following AECOPD

  • Goal: restore a patient to the fullest medical, emotional, social and vocational status possible

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99

What are the 3 main components of pulmonary rehab?

  1. Exercise training (aerobic and resistance exercises)

  2. Nutritional counselling

  3. Patient education

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100

What are important things to educate those with COPD on?

  • Smoking cessation

  • Self-management programs

  • Effective inhaler technique makes sure they are getting the proper amount of drug

  • Early recognition and treatment of acute exacerbations

  • Nutritional counselling

  • Encourage active lifestyle

  • Identify community resources

  • COPD is progressive and there is no cure, when appropriate end of life care should be discussed

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