INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is defined as a disease state characterized by airflow limitation that is not fully reversible .

COPD includes emphysema, an anatomically defined condition

characterized by destruction and enlargement of the lung alveoli;

chronic bronchitis, a clinically defined condition with chronic cough and phlegm; and

small airways disease, a condition in which small bronchioles are narrowed.

GOLD Definitions• The Global Initiative for Chronic Obstructive Lung

Disease (GOLD) defines COPD as follows :

• “Chronic obstructive pulmonary disease (COPD), a common preventable and treatable disease, is characterized by airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients."

Chronic bronchitis

• Chronic bronchitis is defined as a chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough (eg, bronchiectasis) have been excluded .

• It may precede or follow development of airflow limitation.

Emphysema

• Emphysema is defined by abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls, without obvious fibrosis (ie, there is no fibrosis visible to the naked eye)

Risk factors

1.Cigarette smoking

• cigarette smoking- major risk factor for mortality from chronic bronchitis and emphysema.

• FEV1 decreases in a dose- response relationship to the intensity of cigarette smoking, which is typically expressed as pack-years .

• But only 15% of the variability in FEV1 is explained by pack-years.

• This finding suggests that additional environmental and/or genetic factors contribute to the impact of smoking on the development of airflow obstruction.

• 2. Airway Responsiveness and COPD• Many patients with COPD also share feature of airway

hyperresponsiveness (tendency for increased bronchoconstriction in response to a variety of exogenous stimuli, including methacholine and histamine, which is one of the defining features of asthma )

• 3. Respiratory Infections– respiratory infections are important causes of

exacerbations of COPD, the association of both adult and childhood respiratory infections to the development and progression of COPD remains to be proven.

Cont..

4.Occupational exposures -occupational exposures, including coal mining, gold mining, and cotton textile dust, have been suggested as risk factors for chronic airflow obstruction.

5. Ambient air pollution-Prolonged exposure to smoke produced by biomass combustion—a common mode of cooking in some countries—also appears to be a significant risk factor for COPD among women in those countries.

• 6. Passive, or Second-Hand, Smoking Exposure• 7. Genetic Considerations- alpha 1 ANTITRYPSIN

DEFICIENCY-In a small percentage of people, emphysema results from low levels of a protein called alpha-1-antitrypsin (AAt), which protects the elastic structures in lungs from the destructive effects of certain enzymes.

A lack of AAt can lead to progressive lung damage that eventually results in emphysema.

AAt deficiency is a hereditary condition that occurs when patient inherits two defective genes, one from each parent.

PATHOPHYSIOLOGY• Persistent reduction in forced expiratory flow rates is the

most typical finding in COPD. • Increases in the residual volume and the residual

volume/total lung capacity ratio, nonuniform distribution of ventilation, and ventilation-perfusion mismatching also occur. 3 main processes are-

1.Airflow Obstruction- chronically reduced ratio of FEV1/FVC.

2.Hyperinflation-"air trapping" (increased residual volume and increased ratio of residual volume to total lung capacity)

3.Defect in Gas Exchange-PaO2 usually remains near normal until the FEV1 is decreased to ~50% of predicted,

• Decrease in PaCO2 is not expected until the FEV1 is <25% of predicted

Pathology of emphysema • Centriacinar emphysema,

– the type most frequently associated with cigarette smoking, is characterized by enlarged air spaces found (initially) in association with respiratory bronchioles.

– usually most prominent in the upper lobes and superior segments of lower lobes and is often quite focal.

• Panacinar emphysema – refers to abnormally large air spaces evenly

distributed within and across acinar units.– Panacinar emphysema is usually observed in

patients with alpha 1AT deficiency, which has a predilection for the lower lobes.

CLINICAL PRESENTATION

• Three most common symptoms in COPD are – cough,

– sputum production, and

– exertional dyspnea.

• Many patients have such symptoms for months or years before seeking medical attention.

• Although the development of airflow obstruction is a gradual process, many patients date the onset of their disease to an acute illness or exacerbation.

• A careful history, however, usually reveals the presence of symptoms prior to the acute exacerbation.

Physical Findings

• In the early stages of COPD, patients usually have an entirely normal physical examination.

• Current smokers may have signs of active smoking, including an odor of smoke or nicotine staining of fingernails.

• In patients with more severe disease, a prolonged expiratory phase and expiratory wheezing is present.

• In addition, signs of hyperinflation include a barrel chest and enlarged lung volumes with poor diaphragmatic excursion as assessed by percussion.

Cont..

• Patients with severe airflow obstruction may also use accessory muscles of respiration, sitting in the characteristic "tripod" position to facilitate the actions of the sternocleidomastoid, scalene, and intercostal muscles.

• Patients may develop cyanosis, visible in the lips and nail beds.

• As the severity of the airway obstruction increases, physical examination may reveal– hyperinflation (eg, increased resonance to percussion),– decreased breath sounds, – wheezes, – crackles at the lung bases, and/or– distant heart sounds .

• Features of severe disease include an increased anteroposterior diameter of the chest (“barrel-shaped” chest) and a depressed diaphragm with limited movement based on chest percussion.

• Advanced disease may be accompanied by– systemic wasting, with significant weight loss,

– bitemporal wasting, and

– diffuse loss of subcutaneous adipose tissue.

• This syndrome has been associated with both inadequate oral intake and elevated levels of inflammatory cytokines (TNF- ).

• Such wasting is an independent poor prognostic factor in COPD.

• Some patients with advanced disease have paradoxical inward movement of the rib cage with inspiration (Hoover's sign), the result of alteration of the vector of diaphragmatic contraction on the rib cage as a result of chronic hyperinflation.

Cont..

• Signs of overt right heart failure, termed cor pulmonale, are relatively infrequent since the advent of supplemental oxygen therapy.

• Clubbing of the digits is not a sign of COPD, and its presence should alert the clinician to initiate an investigation for causes of clubbing.

• In this population, the development of lung cancer is the most likely explanation for newly developed clubbing.

Lab findings

• Assessment for anemia is an important step in the evaluation of dyspnea.

• Measurement of plasma brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) concentrations is useful as a component of the evaluation of suspected heart failure (HF).

• Among stable COPD patients with normal kidney function, an elevated serum bicarbonate may indirectly identify chronic hypercapnia. In the presence of chronic hypercapnia.

Lab cont..

• Testing for alpha-1 antitrypsin (AAT) deficiency should be obtained in all symptomatic adults with persistent airflow obstruction on spirometry.

• Especially suggestive subsets include the– presence of emphysema in a young individual (eg,

age ≤45 years),– emphysema in a nonsmoker or minimal smoker

– emphysema characterized by predominantly basilar changes on the chest radiograph, or a

– family history of emphysema

Pulmonary function tests

•  Pulmonary function tests, particularly spirometry, are the cornerstone of the– diagnostic evaluation of patients with

suspected COPD. – are used to determine the severity of the airflow

limitation, – assess the response to medications, and– follow disease progression.

PFTS• Spirometry — When evaluating a patient for possible

COPD, spirometry is performed pre and post bronchodilator administration to determine whether airflow limitation is present and whether it is partially or fully reversible.

• Airflow limitation that is irreversible or only partially reversible with bronchodilator is the characteristic physiologic feature of COPD.

• PFTS shows airflow obstruction with a reduction in FEV1 and FEV1/FVC .

• With worsening disease severity, lung volumes may increase, resulting in– an increase in total lung capacity,

– functional residual capacity, and

– residual volume.

• In patients with emphysema, the diffusing capacity (DLCO) may be reduced, reflecting the lung parenchymal destruction characteristic of the disease.

ABG

• The indications for measuring ABGs (eg, arterial oxygen tension [PaO2], carbon dioxide tension [PaCO2], and acidity [pH]), which must be considered in the clinical context, include the following:

• ●Low FEV1 (eg, <50 percent predicted)

• ●Low oxygen saturation by pulse oximetry (eg,SpO2 <92 percent)

• ●Depressed level of consciousness• ●Acute exacerbation of COPD• ●Assessment for hypercapnia in at risk patients 30 to 60

minutes after initiation of supplemental oxygen

Gold Criteria for COPD Severity

CHEST Xray

• Radiographic features suggestive of COPD (usually seen in advanced disease) include:

• Bullae, defined as radiolucent areas larger than 1 cm in diameter. They are due to locally severe disease, and may or may not be accompanied by widespread emphysema

• When advanced COPD leads to pulmonary hypertension and cor pulmonale, prominent hilar vascular shadows and encroachment of the heart shadow on the retrosternal space may be seen

Xray

• Rapidlytapering vascular shadows, increased radiolucency of the lung, a flat diaphragm, and a long, narrow heart shadow

• ●A flat diaphragmatic contour and an increased retrosternal airspace on a lateral radiograph). These findings are due to

hyperinflation.

BODE Index

• APPROXIMATE 4 YEAR SURVIVAL INTERPRETATION• 0-2 Points: 80%• 3-4 Points: 67%• 5-6 Points: 57%• 7-10 Points: 18%

Treatment

Anti smoking therapy• Nicotine replacement therapy– Transdermal

patches, gums, sprays, lozenges, inhalers• Bupropion ( Anti depressant)• Nicotinic receptor partial agonist - Varenicline

• Psychosocial approaches – Cognitive behavioral therapy

VACCINES Influenza vaccines and Pneumococcal polysaccharide

vaccine is recommended for COPD patients • 65 years or more• younger than age 65 with FEV1< 40% predicted

Anticholinergic agents• Ipratropium bromide improves symptoms and

produces acute improvement in FEV1. • Tiotropium, a long-acting anticholinergic, has been

shown to improve symptoms and reduce exacerbations.

• Side effects are minor, and a trial of inhaled anticholinergics is recommended in symptomatic patients with COPD.

Beta agonists

• These provide symptomatic benefit.• The main side effects are tremor and tachycardia.• Long- acting inhaled agonists, such as

salmeterol, have benefits comparable to ipratropium bromide. Their use is more convenient than short-acting agents.

• The addition of a agonist to inhaled anticholinergic therapy has been demonstrated to provide incremental benefit.

Glucocorticoids• A trial of inhaled glucocorticoids should be considered

in patients with frequent exacerbations, defined as two or more per year, and in patients who demonstrate a significant amount of acute reversibility in response to inhaled bronchodilators.

• The chronic use of oral glucocorticoids for treatment of COPD is not recommended because of an unfavorable benefit/risk ratio. The chronic use of oral glucocorticoids is associated with significant side effects, including osteoporosis, weight gain, cataracts, glucose intolerance, and increased risk of infection.

• Theophylline• Theophylline produces modest improvements in expiratory

flow rates and vital capacity

• Nausea is a common side effect; tachycardia and tremor have also been reported.

• Oxygen• Supplemental O2 is the only pharmacologic therapy

demonstrated to unequivocally decrease mortality rates in patients with COPD.

• used for patients with resting hypoxemia (resting O2 saturation 88% or <90% with signs of pulmonary hypertension or right heart failure)

Non pharmacological therapies• Lung volume reduction surgery (LVRS)

is more efficacious than medical therapy among patients with upper-lobe predominant emphysema and low exercise capacity.

• LVRS is costly relative to health-care programs not including surgery.

• In appropriately selected patients with very severe COPD, lung transplantation has been shown to improve quality of life and functional capacity.

EXACERBATIONS OF COPD

• Exacerbations are episodes of increased dyspnea and cough and change in the amount and character of sputum. They may or may not be accompanied by other signs of illness, including fever, myalgias, and sore throat.

Treatment of Exacerbations • Bronchodilators• Typically, patients are treated with an inhaled agonist, often

with the addition of an anticholinergic agent.

• initially with nebulized therapy, as such treatment is often easier to administer in older patients or to those in respiratory distress.

• The addition of methylxanthines (such as theophylline) to this regimen can be considered, although convincing proof of its efficacy is lacking.

• If added, serum levels should be monitored in an attempt to minimize toxicity.

Antibiotics• Patients with COPD are frequently colonized with

potential respiratory pathogens, • Bacteria frequently implicated in COPD exacerbations

include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. In addition, Mycoplasma pneumoniae or Chlamydia pneumoniae are found in 5–10% of exacerbations.

• The choice of antibiotic should be based on local patterns of antibiotic susceptibility of the above pathogens as well as the patient's clinical condition

• .Most practitioners treat patients with moderate or severe exacerbations with antibiotics,

Glucocorticoids

• Among patients admitted to the hospital, the use of glucocorticoids has been demonstrated to reduce the length of stay, hasten recovery, and reduce the chance of subsequent exacerbation or relapse for a period of up to 6 months.

• One study demonstrated that 2 weeks of glucocorticoid therapy produced benefit indistinguishable from 8 weeks of therapy.

• The GOLD guidelines recommend 30–40 mg of oral prednisolone or its equivalent for a period of 10–14 days.

Oxygen

• Supplemental O2 should be supplied to keep arterial saturations 90%. Hypoxemic respiratory drive plays a small role in patients with COPD.

Mechanical Ventilatory Support• Initiation of noninvasive positive-pressure

ventilation (NIPPV) in patients with respiratory failure, defined as PaCO2 >45 mmHg, results in a significant reduction in mortality rate, need for intubation, complications of therapy, and hospital length of stay.

• Invasive (conventional) mechanical ventilation via an endotracheal tube is indicated for patients with severe respiratory distress despite initial therapy, life-threatening hypoxemia, severe hypercarbia and/or acidosis, markedly impaired mental status, respiratory arrest, hemodynamic instability, or other complications.

Difference b/w asthma and COPD

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