copd 2013 with patho
DESCRIPTION
COPD 2013 With PathoCOPD 2013COPD 2013 COPDCOPD 2013 With PathoTRANSCRIPT
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Preventable and treatable disease
with some significant extrapulmonary effects that may contribute to the severity in individual patients
Its pulmonary component is characterized by airflow limitation that is not fully reversible.
(Global Initiative for Chronic Obstructive Lung Disease-GOLD)
COPD
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Emphysema
Chronic bronchitis
COPD
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COPD may include diseases that cause airflow obstruction (eg, emphysema, chronic bronchitis) or any combination of these disorders.
Other diseases such as cystic fibrosis, bronchiectasis, and asthma that were previously classified as types of COPD are now classified as chronic pulmonary disorders.
COPD can coexist with asthma
Death rates continue to rise
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A disease of the airways, is defined as the presence of cough and sputum production for at least 3 months in each of 2 consecutive years.
Although, chronic bronchitis is a clinically and epidemiologically useful term, it does not reflect the major impact of airflow limitation on morbidity and mortality in COPD (GOLD, 2008).
In many cases, smoke or other environmental pollutants irritate the airways, resulting in inflammation and hypersecretion of mucus.
Chronic Bronchitis
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Constant irritation causes the mucus-secreting glands and goblet cells to increase in number, leading to increased mucus production.
Mucus plugging of the airway reduces ciliary function.
Bronchial walls also become thickened, further narrowing the bronchial lumen.
Chronic Bronchitis
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Impaired oxygen and carbon dioxide exchange results from destruction of the walls of overdistended alveoli.
a pathologic term
describes an abnormal distention of the airspaces beyond the terminal bronchioles
and destruction of the walls of the alveoli(GOLD, 2008)
Emphysema
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As the walls of the alveoli are destroyed (a process accelerated by recurrent infections), the alveolar surface area in direct contact with the pulmonary capillaries continually decreases.
This causes an increase in dead space (lung area where no gas exchange can occur) and impaired oxygen diffusion, which leads to hypoxemia.
Emphysema
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Both may occur in the same patient
panlobular (panacinar)
centrilobular (centroacinar)
2 main Types of Emphysema
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there is destruction of the respiratory bronchiole, alveolar duct, and alveolus.
All airspaces within the lobule are essentially enlarged
but there is little inflammatory disease.
panlobular (panacinar)
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A hyperinflated (hyperexpanded) chest, marked dyspnea on exertion, and weight loss typically occur.
To move air into and out of the lungs, negative pressure is required during inspiration, and an adequate level of positive pressure must be attained and maintained during expiration.
Instead of being an involuntary passive act,expiration becomes active and requires muscular effort.
panlobular (panacinar)
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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, polycythemia, and episodes of right-sided heart failure.
This leads to central cyanosis and respiratory failure.
The patient also develops peripheral edema, which is treated with diuretic therapy.
centrilobular (centroacinar)
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Exposure to tobacco smoke (80-90%) Passive smoking Occupational exposure-dust, chemicals Ambient air pollution Genetic abnormalities (deficiency in aplha1-
antitrypsin)
COPD risk factors
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the airflow limitation is both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases
The inflammatory response occurs throughout the:
proximal and peripheral airways lung parenchyma and pulmonary vasculature
Pathophysiology
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In the pulmonary vasculature
In the peripheral airways (bronchioles < 2mm)
In the lung parenchyma (respiratory bronchioles
and alveoli)
Body attempts repair
Airway changes and narrowing occurs
Chronic inflammatory response
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hypoxemia
Scar tissue formation
In the peripheral airways (bronchioles < 2mm)
Narrowing of airway lumen
Thickening of airway wall, fibrosis, exudate formation, further narrowing
Repetitive injury and repair process
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Alveolar wall destruction
In the lung parenchyma (respiratory bronchioles
and alveoli)
Loss of elastic recoil
CO2 retention
hypercapnia
Respiratory acidosis
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In the pulmonary vasculature
Thickening of pulmonary blood vessels
Pulmonary hypertension
Ride sided heart failure
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Chronic bronchitits
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Smoke, air pollution, irritants
CHRONIC IRRITATION
Increase in the number of mucus secreting
glands and goblet cellsinflammation
Adjacent alveoli become damaged
and fibrosed
Increased mucus production
Airflow limitation
Decreased lumen size
Thickened bronchial walls
exacerbation
infection
Increased susceptibility to infection
Altered alveolar macrophage
Reduced ciliary function
Mucus plugging
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Emphyema
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Overdistended alveoli
Alveolar destruction
hypoxemia
Impaired oxygen diffusion
Recurrent infection
Decreased alveolar surface area in contact w/ capillaries
Increased dead space(lung area w/o gas exhange)
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Disease progression
Impaired CO2 elimination
Increased PaCO2
Hypercapnia
Respiratory Acidosis
Increased pulmonary artery pressure (PAP)
Alveolar breakdown continues
Fluid/blood backflows to right ventricle
Decreased size of pulmonary capillary bed
S/Sx of right sided heart failure
RIGHT SIDED HEART FAILURE (COR PULMONALE)
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1. Chronic cough
2. Sputum production
3. Dyspnea on exertion
Worsen over time; progressive
3 primary symptoms
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Chronic cough and sputum production often precede the development of airflow limitation by many years.
However, not all people with cough and sputum production develop COPD
The cough may be intermittent and may be unproductive in some patients
Clinical Manifestations
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Dyspnea at rest (as COPD progresses)
Weight loss (common, dyspnea interferes w/ eating, labored breathing is also energy depleting)
Use of accessory muscles (for breathing)
Clinical manifestations
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chronic hyperinflation leads to the “barrel chest” thorax configuration
results from a more fixed position of the ribs in the inspiratory position (due to hyperinflation)
Retraction of the supraclavicular fossae occurs on inspiration, causing the shoulders to heave upward
the abdominal muscles may also contract on inspiration (advanced emphysema)
Clinical manifestation in emphysema
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Chronic Bronchitis Pulmonary Emphysema•“Blue Bloaters” (cyanosis with edema) •“Pink puffers” (acyanotic with compensatory
pursed-lip breathing)
•Inflammation of the Bronchi, which causes increased mucus production (by goblet cells) and chronic cough
•Destruction of alveolar wall leading to permanent overdistention of dead air spaces (blebs and bullae); Alpha 1 antitrypsin Deficiency
•Bronchioles narrowed as a result of thickened membrane and with inflammation of surrounding tissue
•Lung tissue becomes inelastic and lungs enlarge with small bronchioles collapse that lead to air trapping
•Persistent cough, copious sputum production, dyspnea, shortness of breath
•(+) of cough and sputum production for at least 3 months in each of 2 consecutive years•persistent SOB•progressive dyspnea•diminished breath sounds•barrel chest
•“Dirty Lung” appearance in chest X-ray •Overinflated lucent lungs in X-ray
•Enlarged heart (cor pulmonale-right ventricle)
•Late cor pulmonale
•Increased PaCO2; hypoxemia usually present
•Low PaCO2 (usually); mild to mod. hypoxemia
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COPD is classified into four stages depending upon the severity (measured by pulmonary function tests) and symptoms (GOLD, 2008).
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Stage I (mild)◦ defined by an FEV1/FVC less than 70% and an FEV1
greater than or equal to 80% predicted, and the patient may be with or without symptoms of cough and sputum production.
Stage II (moderate)◦ defined by an FEV1/FVC less than 70%, an FEV1 50% to
80% predicted, and shortness of breath typically developing upon exertion.
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Stage III (severe)◦ defined as an FEV1/FVC less than 70% and an FEV1 less
than 30% to 50% predicted◦Severe COPD symptoms include increased shortness of
breath, reduced exercise capacity, and repeated exacerbations.
stage IV (very severe)◦ defined as an FEV1/FVC less than 70%, an FEV1 less
than 30% to 50% predicted,
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Questions???
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Spirometry (reduced FEV1) Spirometry bronchodilator spirometry (degree of reversibility)
ABG -arterial blood gas (O2 & gas ex)
PFT-pulmonary function test
X-ray & High resolution CT scan (r/o other diseases)
screening for alpha1-antitrypsin deficiency (younger than 45)
Diagnostics
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Respiratory insufficiency and failure (Major) pneumonia chronic atelectasis pneumothorax and pulmonary arterial hypertension/Right sided
heart failure (cor pulmonale)
Complications
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Risk reduction (Smoking cessation-most effective)
Bronchodilators◦ Via metered dose inhaler (MDI), other inhalers,
nebulization, oral◦ Both regular and PRN◦ beta-adrenergic agonists (short- and long-acting◦Anticholinergic agents (short- and long-acting)◦methylxanthines◦ and combination agents
Corticosteroids
Medical management
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For stage I (mild) COPD, a short-acting bronchodilator may be prescribed.
For stage II or III COPD, a short-acting bronchodilator along with regular treatment of one or more long-acting bronchodilators may be used.
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For stage III or IV (severe or very severe) COPD,
medication therapy includes regular treatment with one or more bronchodilators and inhaled corticosteroids for repeated exacerbations.
Combination long-term beta2-agonists plus corticosteroids in one inhaler may be appropriate; examples include formoterol/budesonide (Symbicort) and salmeterol/fluticasone (Seretide).
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Others: Alpha1-antitrpsin augmentation therapy Antibiotic Mucolytic Antitussive Vasodilators Narcotics Vaccines (for influenza) Oxygen therapy
Medical management
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can be administered as: long-term continuous therapy during exercise to prevent acute dyspnea during an exacerbatio.
Oxygen therapy
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increase the baseline resting (PaO2) to at least 60 mm Hg at sea level
and an arterial oxygen saturation (SaO2) at least 90%
Goal of Oxygen therapy
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Administering too much oxygen can result in the retention of carbon dioxide.
Oxygen therapy is variable in COPD patients; its aim in COPD is to achieve an acceptable
oxygen level without a fall in the pH (increasing hypercapnia).
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Bullectomy surgical option for select patients with bullous
emphysema. Bullae are enlarged airspaces
Surgical Management
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Lung volume Reduction surgery a palliative surgical option Removal of a portion of the diseased lung
parenchyma Reduces hyperinflation and allows the functional
tissue to expand
Surgical Management
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Lung transplantation
improve quality of life and functional capacity
Limited not only by the shortage of donor organs
it is also a costly procedure with financial implications for months to years because of complications and the need for costly immunosuppressive medication regimens
Surgical Management
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Reduce risk factors Health education Breathing Exercises Activity Pacing Self-Care Activities Physical Conditioning Oxygen Therapy Nutritional Therapy Coping Measures
Pulmonary Rehabilitation (p.611)
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Assessing the Patient Achieving Airway Clearance Improving Breathing Patterns Improving Activity Tolerance Monitoring and Managing Potential Complications Promoting Home and Community-Based Care
Nursing Management (p.612)
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Ideal for stage 2-4 Minimum 6 weeks The longer the better Smoking cessation is very important◦Set goal with the client regarding ‘quit date’◦ Follow up about 3 to 5 days if client did stop◦Refer if needed◦ Focus on achievements and strengths, not negatives
Pulmo rehab notes
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Diaphragmatic breathing is taught◦which reduces the respiratory rate, increases alveolar ventilation◦ and sometimes helps expel as much air as possible during
expiration
Pursed lip breathing◦ helps slow expiration◦ prevents collapse of small airways◦ helps patient control the rate and depth of respiration◦ promotes relaxation, enabling the patient to gain control of
dyspnea and reduce feelings of panic
Pulmo rehab notes
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Questions???