chronic obstructive pulmonary disease
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Chronic Obstructive Pulmonary Disease (COPD)
is a major cause of chronic morbidity and mortality throughout the world. Many
people suffer from this disease for years and die prematurely from it or its
complications. COPD is the fourth leading cause of death in the world, and further
increases in its prevalence and mortality can be predicted in the coming decades.
Researchers estimate the prevalence of chronic airflow obstruction in the world as
4-6%.
Chronic Obstructive Pulmonary Disease (COPD) is a 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. The airflow limitation is usually
progressive and associated with an abnormal inflammatory response
of the lung to noxious particles or gases. The chronic airflow limitation
characteristic of COPD is caused by a mixture of small airway disease (obstructive
bronchiolitis) and parenchymal destruction (emphysema), the relative contributions
of which vary from person to person.
Etiology
Tobacco Smoke:
Cigarette smoking is by far the most commonly encountered risk factor for COPD.
Cigarette smokers have a higher prevalence of respiratory symptoms and lung
function abnormalities, a greater annual rate of decline in FEV1, and a greater
COPD mortality rate than nonsmokers. Pipe and cigar smokers have greater COPD
morbidity and mortality rates than nonsmokers, although their rates are lower than
those for cigarette smokers. Other types of tobacco smoking popular in various
countries are also risk factors for COPD. Although their risk relative to cigarette
smoking has not been reported. The risk for COPD in smokers is dose-related. Age
at starting to smoke, total pack-years smoked, and current smoking status are
predictive of COPD mortality. Not all smokers develop clinically significant
COPD, which suggests that genetic factors must modify each individual’s risk.
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Occupational Dusts and Chemicals:
Occupational exposures are an underappreciated risk factor for COPD. These
exposures include organic and inorganic dusts and chemical agents and fumes. The
most dangerous combination is work in a harmful environment and smoking.
An infectious factor is considered the second, which joins later, when
special conditions appear – on a background of chronic cough with
expectoration , favourable to infecting of bronchial tree.
COPD is a polygenic disease and a classic example of gene-environment
interaction. The genetic risk factor that is best documented is a severe
hereditary deficiency of alpha-1 antitrypsin. A significant familial risk of
airflow obstruction has been observed in smoking siblings of patien with
severeCOPD, suggesting that genetic factors could influence this
susceptibility.
Pathogeny
chronic inflammation of bronchial tubes, parenchyma and lungs
Oxidative Stress
Protease-Antiprotease Imbalance
Pathological changes characteristic of COPD are found in the proximal airways,
peripheral airways, lung parenchyma,and pulmonary vasculature. The pathological
changes include chronic inflammation, with increased numbers of specific
inflammatory cell types in different parts of the lung, and structural changes
resulting from repeated injury and repair. In general, the inflammatory and
structural changes in the airways increase with disease severity.
CLINICAL PRESENTATION
The characteristic symptoms of COPD are chronic and progressive dyspnea,
cough, and sputum production. Chronic cough and sputum production may precede
the development of airflow limitation by many years.
Cough. Chronic cough, often the first symptom of COPD, is often discounted by
the patient as an expected consequence of smoking and/or environmental
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exposures. Initially, the cough may be intermittent, but later is present
every day, often throughout the day. The chronic cough in COPD may be
unproductive. In some cases, significant airflow limitation may develop without
the presence of a cough..
Sputum production. COPD patients commonly raise small quantities of tenacious
sputum after coughing. Regular production of sputum for 3 or more months in 2
consecutive years (in the absence of any other conditions that may explain it) is the
epidemiological definition of chronic bronchitis).
Dyspnea. Dyspnea, the hallmark symptom of COPD, is the reason most patients
seek medical attention and is a major cause of disability and anxiety associated
with the disease. Typical COPD patients describe their dyspnea as a sense of
increased effort to breathe, heaviness,air hunger.
DIAGNOSTICS
Central cyanosis, or bluish discoloration of the mucosal membranes, may be
present but is difficult to detect in artificial light and in many racial groups.
Common chest wall abnormalities, which reflect the pulmonary
hyperinflation seen in COPD, include relatively horizontal ribs, “barrel-
shaped” chest, and protruding abdomen. Resting respiratory rate is often
increased to more than 20 breaths per minute and breathing can be relatively
shallow. Ankle or lower leg edema can be a sign of right heart failure.
Palpation and percussion.
• These are often unhelpful in COPD.
• Detection of the heart apex beat may be difficult due to pulmonary
hyperinflation.
• Hyperinflation also leads to downward displacement of the liver and an increase
in the ability to palpate this organ without it being enlarged.
Auscultation.
• Patients with COPD often have reduced breath sounds, but this finding is not
sufficiently characteristic to make the diagnosis19.
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• The presence of wheezing during quiet breathing is a useful pointer to airflow
limitation. However, wheezing heard only after forced expiration has not been
validated as a diagnostic test for COPD.
• Inspiratory crackles occur in some COPD patients but are of little help
diagnostically.
• Heart sounds are best heard over the xiphoid area.
Lung function tests
show evidence of airflow limitation. The ratio of the FEV1 to the FVC is reduced
and the PEFR is low. In many patients the airflow limitation is reversible to some
extent (usually a change in FEV1 of < 15%), and the distinction between asthma
and COPD can be difficult. Lung volumes may be normal or increased, and the gas
transfer coefficient of carbon monoxide is low when significant emphysema is
present
Chest X-ray
is often normal, even when the disease is advanced. The classic features are the
presence of bullae, severe overinflation of the lungs with low, flattened
diaphragms, and a large retrosternal air space on the lateral film. There may also be
a deficiency of blood vessels in the periphery of the lung fields compared with
relatively easily visible proximal vessels
Haemoglobin level and PCV
can be elevated as a result of persistent hypoxaemia (secondary polycythaemia,
Blood gases
are often normal. In the advanced case there is evidence of hypoxaemia and
hypercapnia
Sputum examination
is unnecessary in the ordinary case as Strep. pneumoniae or H. influenzae are
the only common organisms to produce acute exacerbations.
CLASSIFICATION
Stages of COPD
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The impact of COPD on an individual patient depends not just on the degree of
airflow limitation, but also on the severity of symptoms (especially breathlessness
and decreased exercise capacity). There is only an imperfect relationship between
the degree of airflow limitation and the presence of symptoms. Spirometric
staging,therefore, is a pragmatic approach aimed at practical implementation and
should only be regarded as an educational tool and a general indication to the
initial approach to management.
Stage I: Mild COPD - Characterized by mild airflow limitation (FEV1/FVC <
0.70; FEV1 ≥80% predicted).Symptoms of chronic cough and sputum production
may be present, but not always. At this stage, the individual is usually unaware that
his or her lung function is abnormal.
Stage II: Moderate COPD - Characterized by worsening airflow limitation
(FEV1/FVC < 0.70; 50% ≤FEV1 < 80% predicted), with shortness of breath
typically developing on exertion and cough and sputum production sometimes also
present. This is the stage at which patients typically seek medical attention because
of chronic respiratory symptoms or an exacerbation of their disease.
Stage III: Severe COPD - Characterized by further worsening of airflow limitation
(FEV1/FVC < 0.70; 30% ≤FEV1 < 50% predicted), greater shortness of breath,
reduced exercise capacity, fatigue, and repeated exacerbations that almost always
have an impact on patients’ quality of life.
Stage IV: Very Severe COPD - Characterized by severe airflow limitation
(FEV1/FVC < 0.70; FEV1 < 30% predicted or FEV1 < 50% predicted plus the
presence of chronic respiratory failure). Respiratory failure is defined as an arterial
partial pressure of O2 (PaO2) less than 8.0 kPa (60 mm Hg), with or without
arterial partial pressure of CO2 (PaCO2) greater than 6.7 kPa (50 mm Hg)
whilebreathing air at sea level.
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Differential diagnostics
For differential diagnostics of COPD with other bronchopulmonary diseases use
bronchoscopy , if necessary – biopsy.
Testimonies to bronchoscopy :
1) suspicion on a neoplasty process ;
2) intrabronchia foreign body ;
3) congenital anomalies of the respiratory system, tuberculosis of bronchial
tubes and lymphatic glands ;
4) bronchiectasis, abscess of lungs;
5) hemoptysis, pulmonary bleeding;
6) bronchial asthma in combination with a bronchitis, pneumonia;
7) with the purpose of sanation of bronchial tubes.
Contra-indications:
1) stenocardia;
2) acute myocardial infarction ;
3) chronic decompensated pulmonary heart;
4) General severe condition of patient.
Bronchography is used for diagnostics of multiple bronchiectasis.
Main reason of late diagnostics of COPD is absence of possibility of timely
research of FVD.
PHARMACOLOGIC TREATMENT
Pharmacologic therapy is used to
prevent and control symptoms,
reduce the frequency and severity of exacerbations,
improve health status, and
improve exercise tolerance.
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Drug Category: Bronchodilators
These agents act to decrease muscle tone in both small and large airways in the
lungs, thereby increasing ventilation. Category includes subcutaneous medications,
beta-andrenergics, methylxanthines, and anticholinergics.
Bronchodilator medications are central to symptom management in COPD.
Inhaled therapy is preferred. The choice between _2-agonist, anticholinergic,
theophylline, or combination therapy depends on availability and individual
response in terms of symptom relief and side effects. Bronchodilators are
prescribed on an as-needed or on a regular basis to prevent or reduce symptoms.
Long-acting inhaled bronchodilators are more effective and convenient.
Combining bronchodilators may improve efficacy and decrease the risk of side
effects compared to increasing the dose of a single bronchodilator.
Inhaled bronchodilators
Drugs Dose (mcg) Duration of
action
short-acting beta-agonists:
salbutamol (Ventolinum),
Fenoterol(Berotek).
100
100
4-6
4-6
short-acting cholinergic antagonist:
Ipratropiya bromide (Ipravent) 20, 40 6-8
Combined drugs
(short-acting beta-agonists +
short-acting cholinergic antagonist:
Fenoterol + Ipratropiya bromide (berodual)
salbutamol + Ipratropiya bromide (combivent)
Long-acting inhaled β2-agonists
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Salmeterol (Serevent)
Formoterol (Zafiron)
25, 50
4, 12
12
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Long-acting cholinergic antagonist
Tiotropiya bromide (Spiriva) 18 24
Theophylline and its various salts are medium-potency bronchodilators with
questionable anti-inflammatory propertie.
For maintenance therapy, long-acting theophylline compounds are available and
are usually given once or twice daily. Single-dose administration in the evening
reduces nocturnal symptoms and helps keep the patient complaint-free during the
day. They are now considered second-line therapy, and as such they are rarely used
in acute situations and infrequently in chronic ones.
Drug Category: Corticosteroids
A recent meta-analysis of 16 controlled trials in stable COPD found that
approximately 10% of patients respond to these drugs. The responders should be
identified carefully. An increase in FEV1 >20% is used as surrogate marker for
steroid response. In acute exacerbation, steroids improve symptoms and lung
functions. Inhaled steroids have fewer adverse effects compared to oral agents.
Although effective, these agents improve expiratory flows less effectively than oral
preparations, even at high doses. These agents may be beneficial in slowing rate of
progression in a subset of patients with COPD who have rapid decline
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Antibiotics
In patients with COPD, chronic infection or colonization of the lower
airways is common from Streptococcus pneumoniae, Haemophilus influenzae, and
Moraxella catarrhalis.
Empiric antimicrobial therapy must be comprehensive and should cover all
likely pathogens in the context of the clinical setting. The goal of antibiotic therapy
in COPD is not to eliminate organisms but to treat acute exacerbations.
Exacerbations are indicated by increased sputum purulence and volume and the
development of dyspnea along with other features, including fever, leukocytosis, or
infiltrate on a chest radiograph.
The first-line treatment choices include amoxicillin, or cefaclor.
Second-line antibiotic regimens are the more expensive antibiotics, including
azithromycin, clarithromycin, and fluoroquinolones.
The use of antibiotics in patients with COPD is supported by the results of a meta-
analysis showing that patients who received oral antibiotic therapy had a small, but
clinically significant, improvement in peak expiratory flow rate and a more rapid
resolution of symptoms. Patients who benefitted most were those whose
exacerbations were characterized by at least 2 of the following: increases in
dyspnea, sputum production, and sputum purulence.
Mucolytic agents
These agents reduce sputum viscosity and improve secretion clearance. Viscous
lung secretions in patients with COPD consist of mucous-derived glycoproteins
and leukocyte-derived DNA.
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The oral agent N-acetylcysteine has antioxidant and mucokinetic properties and is
used to treat patients with COPD. However, the efficacy of mucolytic agents in the
treatment of COPD is debatable.
Complications
Respiratory failure is a syndrome in which the respiratory system fails in one
or both of its gas exchange functions: oxygenation and carbon dioxide elimination.
In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg
while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, respiratory
failure may be acute or chronic. While acute respiratory failure is characterized by
life-threatening derangements in arterial blood gases and acid-base status, the
manifestations of chronic respiratory failure are less dramatic and may not be as
readily apparent.
The cause of respiratory failure often is evident after a careful history and
physical examination.
o Cardiogenic pulmonary edema usually develops in the context of a
history of left ventricular dysfunction or valvular heart disease.
o A history of previous cardiac disease, recent symptoms of chest pain,
paroxysmal nocturnal dyspnea, and orthopnea suggest cardiogenic
pulmonary edema.
o Noncardiogenic edema (eg, acute respiratory distress syndrome
[ARDS]) occurs in typical clinical contexts such as sepsis, trauma,
aspiration, pneumonia, pancreatitis, drug toxicity, and multiple
transfusions.
Classification of RF is based on clinical features:
RF has three degrees of severity:
- I degree - patient feels appearance of shortbreathing during the usual
physical exercises (the level of such exercises is individual for every patient and
depends on physical development);
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- II degree -shortbreathing appears during the insignificant physical
exercises (for example, at walking on an plane surface);
- III degree -shortbreathing is observed in a state of rest.
Pulmonary rehabilitation
o Many patients with COPD are unable to enjoy life to the fullest
because of shortness of breath, physical limitations, and inactivity.
o Pulmonary rehabilitation encompasses an array of therapeutic
modalities designed to improve the patient's quality of life by
decreasing airflow limitation, preventing secondary medical
complications, and alleviating respiratory symptoms.
o The 3 major goals of the comprehensive management of COPD are
the following:
1. Lessen airflow limitation
2. Prevent and treat secondary medical complications (eg,
hypoxemia, infection)
3. Decrease respiratory symptoms and improve quality of life
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