3. At the end of this section learner will be able to:
Define chronic obstructive pulmonary disease
Understand the risk factors of COPD
Explain the pathophysiology of COPD
Identify the clinical manifestation
Understand the diagnosis and management
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5. COPD is a common, preventable and treatable disease
that is characterized by persistent respiratory symptoms
and airflow limitation that is
Due to airway and/or alveolar abnormalities
Usually caused by significant exposure to noxious
particles or gases and influenced by host factors
including abnormal lung development
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6. It is a progressive disease that makes hard to breathe,
due to long-term damage that weakens or collapses the
air sacs between the lungs.
It includes:
1) Chronic bronchitis
2) Emphysema
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7. It is most common in adults who are current or former
cigarette smokers.
The prevalence of COPD is two to three times higher in
people over the age of 60 years than in younger age
groups
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8. Chronic bronchitis is ongoing inflammation of the
bronchi (airways in the lungs).
Due to the inflammation , the airways produce extra
mucus. This can cause cough and make it hard to
breathe.
It is defined clinically as the presence of a chronic
productive cough for 3 months during each of 2
consecutive years (other causes of cough being
excluded). 4/25/2024
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10. Emphysema is defined pathologically as an abnormal,
permanent enlargement of the air spaces distal to the terminal
bronchioles, accompanied by destruction of their walls
It is where the air sacs in the lungs (alveoli) are damaged.
Over time, the walls of air sacs are destroyed, creating larger
spaces.
This reduces the surface area of the lungs and makes the lungs
less efficient.
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11. There are two main types of emphysema, based on the
changes taking place in the lung:
panlobular (panacinar)
Centrilobular(centroacinar)
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12. In the centrilobular (centroacinar),
pathologic changes take place mainly in the center of
the secondary lobule, preserving the peripheral portions
of the acinus.
Frequently, there is a derangement of ventilation–
perfusion ratios
producing chronic hypoxemia, hypercapnia (increased
CO2 in the arterial blood), polycythemia,
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13. In the panlobular (panacinar)
there is destruction of the respiratory bronchiole,
alveolar duct, and alveoli.
All air spaces within the lobule are essentially enlarged
hyperinflated (hyperexpanded) chest (barrel chest on
physical examination),
marked dyspnea on exertion
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16. Host Factors
Genes (alpha1- anti-trypsin↓)
Hyper responsiveness
low BW, Age
Exposure
Tobacco smoke,
Biomass fuel smoke, open fires.wood
Occupational dusts and chemicals
Chronic uncontrolled asthma
Low socioeconomic status,
Low dietary vegetable and fruit intake
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17. A history of childhood respiratory infections
Exposure to secondhand smoke
People with a history of asthma
People who have underdeveloped lungs
Those who are age 40 and older as lung function decline
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18. Childhood respiratory disease, maltreatment, maternal
smoking and low birth weight increase the risk of
COPD. Promising advances in prevention strategies for
early life exposures could markedly decrease the risk of
COPD.
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19. COPD results from the combined processes of peripheral
airway inflammation and narrowing of the airways. this leads
to airflow limitation
The destruction alveoli, terminal bronchioles and surrounding
capillary vessels and tissues, which adds to airflow limitation
and leads to decreased gas transfer capacity
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20. The extent of airflow limitation is determined by the
severity of inflammation, development of fibrosis
within the airway and presence of secretions or
exudates.
Reduced airflow on exhalation leads to air trapping,
resulting in reduced inspiratory capacity,
which may cause breathlessness (dyspnea) on
exertion and reduced exercise capacity. 4/25/2024
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21. Abnormalities in gas transfer occur due to reduced
airflow/ventilation and as a result of loss of alveolar structure
and pulmonary vascular bed.
Low oxygen blood levels (hypoxemia) and raised blood
carbon dioxide levels (hypercapnia) result from impaired gas
transfer
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23. Health History and Physical Exam
Respiratory symptoms, including:
dyspnea (progressive, persistent and worse
with exercise);
chronic cough; and
increased sputum production
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24. Current or past smoking history
Exposure to secondhand smoke; air pollution; prior
history working with chemicals, dust or fumes; and a
history of childhood respiratory infection
Family members diagnosed with COPD, alpha-1
deficiency or another chronic lung disease
Times when symptoms get worse such as change of
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25. Pulmonary function test (spirometry)
Alpha-1testing
Chest x-ray
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27. Goal of management:
Prevent disease progression
Relieve symptoms
Improve exercise tolerance
Improve health status
prevent and treat complication
Prevent and treat exacerbation
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28. Implement pharmacologic therapy in a stepwise
approach and
use the lowest step that achieves optimal control based
on the patient’s severity of COPD
When assessing for the next step, consider exertional
dyspnea, functional status, history of exacerbations,
patient preference (e.g., cost and ability to adhere to
treatment plan) and occurrence of adverse effects
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30. For symptom relief
For all symptomatic patients, prescribe a short-acting
inhaled bronchodilator (short-acting beta2-agonist)
(SABA) or short acting muscarinic antagonist (SAMA)
for acute, short-term relief of shortness of breath.
For those with moderate COPD, SAMA or SABA
monotherapy is recommended.
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31. SAMA reduces the risk of AECOPD, improves quality
of life and lung function, and may be better tolerated,
as compared to SABA monotherapy.
If symptoms are not well controlled with monotherapy,
consider combination therapy of SAMA + SABA
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32. For symptom relief and to prevent exacerbations
At the next step in symptom management, consider
monotherapy with a long-acting beta2-agonist (LABA)
or a long-acting muscarinic antagonist (LAMA).
If monotherapy does not provide adequate relief of
symptoms, consider a combination of LABA + LAMA,
which provides slightly better quality life and lung
function over either therapy alone, and reduces
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33. To prevent exacerbations
For those with moderate to severe COPD and repeated
exacerbations (e.g., FEV1 < 50% predicted and
≥ 2 exacerbations in the past 12 months),
a triple combination therapy of a LABA + ICS and
LAMA is recommended.
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35. Acute exacerbations are characterized by sustained (
48 hours or more) worsening of shortness of breath and
coughing, usually with increasing sputum volume.
The most common cause of AECOPD is a viral or
bacterial infection
non-infectious causes of exacerbations including:
pleural effusion, heart failure, pulmonary embolism,
and pneumothorax. 4/25/2024
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37. Bronchodilators
Inhaled B2 agonist, often with the addition of an
anticholinergic agent.
Oxygen
Supplemental O2 should be supplied to keep arterial saturations
90%.
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38. Lung cancer
Corpulmonale
Depression and Anxiety
respiratory failure
pneumothorax.
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39. Maintaining Patent Airway Clearance
Promoting Effective Gas Exchange & Oxygen Therapy
Improving Breathing Pattern Through Breathing
Exercises
Promoting Infection Control & Preventing
Complications
Promoting Optimal Nutrition Balance
Promoting Rest and Tolerance to Activity 4/25/2024
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40. <GOLD-2024_v1.1-1Dec2023_WMV.pdf>.
<COPD guideline diagnosis and
manangement,2017.pdf>.
Ribeiro, J. D., & Fischer, G. B. (2015). Chronic
obstructive pulmonary diseases in children. J Pediatr
(Rio J), 91(6 Suppl 1), S11-25.
Bush, A. (2008). COPD: a pediatric disease. COPD,
5(1), 53-67.
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COPD is an umbrella term for the conditions emphysema, chronic bronchitis and long-standing asthma. While these conditions can all have similar symptoms, they have different effects on the lungs:
To understand COPD, it helps to understand how the lungs work. The air that you breathe goes down your windpipe into tubes in your lungs called bronchial tubes or airways. The airways are shaped like an upside-down tree with many branches.
At the end of the branches are tiny air sacs called alveoli (al-VEE-uhl-eye).
Small blood vessels called capillaries run through the walls of the air sacs. When air reaches the air sacs, the oxygen in the air passes through the air sac walls into the blood in the capillaries. At the same time, carbon dioxide (a waste gas) moves from the capillaries into the air sacs. This process is called gas exchange.
The airways and air sacs are elastic (stretchy). When you breathe in, each air sac fills up with air like a small balloon. When you breathe out, the air sacs deflate and the air goes out.
In COPD, less air flows in and out of the airways because of one or more of the following: The airways and air sacs lose their elastic quality. The walls between many of the air sacs are destroyed. The walls of the airways become thick and inflamed. The airways make more mucus than usual, which tends to clog them
Emphysema (loss of alveolar structure); l Chronic bronchitis (long-term inflammation of the airways and mucus hyper-secretion).
Chronic bronchitis is well recognized in adults, formally defined as 3 mo or longer of productive cough each year for 2 or more yr. The disease can develop insidiously, with episodes of acute obstruction alternating with quiescent periods. Some predisposing conditions can lead to progression of airflow obstruction or chronic obstructive pulmonary disease, with smoking as the major factor (up to 80% of patients have a smoking history). Other conditions include air pollution, occupational exposures, and repeated infections. In children, cystic fibrosis, bronchopulmonary dysplasia, and bronchiectasis must be ruled out. The applicability of this definition to children is unclear. The existence of chronic bronchitis as a distinct entity in children is controversial. Like adults, children with chronic inflammatory diseases or those with toxic exposures can develop damaged pulmonary epithelium. Thus chronic or recurring cough in children should lead the clinician to search for underlying pulmonary or systemic disorders (see Table 418.3 ). One proposed entity that shares characteristics with asthma and other forms of suppurative lung disease is persistent or protracted bacterial bronchitis. Protracted bacterial bronchitis is defined as a chronic (>3 wk) wet cough, characterized by bacterial counts of 10 4 colony-forming units/mL or greater from bronchoalveolar lavage and resolution of cough within 2 wk of treatment with antimicrobial therapy. nelson
Pathophysiology of chronic bronchitis as compared to a normal bronchus. The bronchus in chronic bronchitis is narrowed and has impaired air flow due to multiple mechanisms: inflammation, excess mucus production, and potential smooth muscle constriction (bronchospasm
This leads to central cyanosis, peripheral edema, and respiratory failure. The patient may receive diuretic therapy for edema
polycythemia: increase in the red blood cell concentration in the blood; in COPD, the body attempts to improve oxygen carrying capacity by producing increasing amounts of red blood cells
The patient with this type of emphysema typically has a
Changes in alveolar structure in centrilobular and panlobular emphysema. In panlobular emphysema, the bronchioles, alveolar ducts, and alveoli are destroyed and the air spaces within the lobule are enlarged. In centrilobular emphysema, the pathologic changes occur in the lobule, while the peripheral portions of the acinus are preserved
Emphysema (loss of alveolar structure); l Chronic bronchitis (long-term inflammation of the airways and mucus hyper-secretion).
A genetic condition called AAT (alpha-1 antitrypsin) deficiency increases the risk of developing COPD at any age. According to the National Heart, Lung, and Blood Institute, up to 100,000Trusted Source people in the U.S. may have AAT deficiency.
AAT deficiency makes it difficult for the body to respond to damage in the lungs, which could lead to people with the deficiency developing COPD faster than others.
In these cases, people may have never been smokers or had exposure to harmful chemicals and pollutants, but they will still be at high risk for COPD.
While these causes and risk factors may increase your risk of developing COPD, people living in poverty and people living in rural areas are more likely to develop COPD. Beyond smoking status, some reasons for the increased risk of developing COPD may include exposures to indoor and outdoor pollutants, occupational exposures and lack of access to healthcare. COPD is often referred to as a "smoker’s disease" however although smoking is one of the main risk factors for developing COPD, people who never smoke may also develop COPD. Other risk factors may include:
The primary or initiating factor in the genesis of chronic bronchitis is exposure to noxious or irritating inhaled substances such as tobacco smoke (90% of patients are smokers) and dust from grain, cotton, and silica. Chronic bronchitis
Mucus hypersecretion.
The earliest feature of chronic bronchitis is hypersecretion of mucus in the large airways,
associated with hypertrophy of the submucosal glands in the trachea and bronchi.
enetic factors: a small number of people have a form of emphysema caused by a protein disorder called alpha-1 antitrypsin deficiency (AATD). This is where the body finds it difficult to produce one of the proteins (Alpha-1 antitrypsin) which usually protects the lungs. The lack of this protein can make a person more susceptible to lung diseases such as COPD
Clinical Manifestations COPD is characterized by three primary symptoms: cough, sputum production, and dyspnea on exertion (NIH, 2001). These symptoms often worsen over time. Chronic cough and sputum production often precede the development of airflow limitation by many years. However, not all individuals with cough and sputum production will develop COPD. Dyspnea may be severe and often interferes with the patient’s activities. Weight loss is common because dyspnea interferes with eating, and the work of breathing is energy-depleting. Often the patient cannot participate in even mild exercise because of dyspnea; as COPD progresses, dyspnea occurs even at rest. As the work of breathing increases over time, the accessory muscles are recruited in an effort to breathe. The patient with COPD is at risk for respiratory insufficiency and respiratory infections, which in turn increase the risk for acute and chronic respiratory failure. In COPD patients with a primary emphysematous component, chronic hyperinflation leads to the “barrel chest” thorax configuration. This results from fixation of the ribs in the inspiratory position (due to hyperinflation) and from loss of lung elasticity (Fig. 24-3). Retraction of the supraclavicular fossae occurs on inspiration, causing the shoulders to heave upward (Fig. 24-4). In advanced emphysema, the abdominal muscles also contract on
history of exposure to cigarette smoke; • history of environmental/occupational exposure to smoke, dust or gas/fumes; • frequent respiratory infections; or • family history of COPD.
The most common lung function test is called spirometry. A spirometry test can diagnose COPD. A spirometer can measure the amount and speed of the air you blow out. This helps your healthcare provider see how well your lungs are working.
: COPD = chronic obstructive pulmonary disease; ICS = inhaled corticosteroid; LABA = long-acting beta2-agonist; LAMA = long-acting muscarinic antagonist; SABA = short-acting beta2-agonist; SAMA = short-acting muscarinic antagonist.
Long acting muscarinic receptor antagonists (LAMA) reverse airflow obstruction by antagonizing para-sympathetic bronchoconstricting effects within the airways. For years, tiotropium, has been the cornerstone LAMA for chronic obstructive pulmonary disease (COPD) management.
Muscarinic antagonists increase airflow in COPD by blocking cholinergic tone at airway smooth muscle.
n chronic obstructive pulmonary disease (COPD) and asthma, cholinergic mechanisms contribute to increased bronchoconstriction and mucus secretion that limit airflow.
Fixed dose combination inhalers of LABA with a LAMA are available and have been shown to be superior to inhaled corticosteroid (ICS) + LABA combination in reducing symptoms and preventing exacerbations in
Fixed dose combination inhalers of an ICS with a LABA are available;
if a combination inhaler is initiated, discontinue the use of the single agent LABA inhaler
Exacerbations of chronic obstructive pulmonary disease (COPD) have a high rate of mortality which gets worse with advancing age
Lung cancer — COPD may increase the risk of lung cancer
Cor pulmonale is right-sided heart failure secondary to long-standing COPD. It is caused by chronic hypoxia and subsequent vasoconstriction in pulmonar
Depression and Anxiety ... At least 1 in 10 people with early COPD get depression or anxiety, and that number climbs as the disease gets worse. Medication can ...y
Chronic respiratory failure
-- a complication of end-stage COPD -- is defined as persistently elevated carbon dioxide and, usually, recurrent episodes of acute ...
pneumothorax.
variable. medium. Occurs because of lung parenchyma damage with sub-pleural bulla formation and rupture
