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Chronic obstructive pulmonary disease (COPD)

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Title: Chronic obstructive pulmonary disease (COPD)


1
Chronic obstructive pulmonary disease (COPD)
2
  • Definition
  • COPD is a disease state characterized by airflow
    limitation that is not fully reversible.
  • The airflow limitation is usually both
    progressive and associated with an abnormal
    inflammatory response of the lungs to noxious
    particles or gases.

3
Epidemiology and aetiology
  • COPD is caused by long-term exposure to toxic
    particles and gases.
  • In developed countries, cigarette smoking
    accounts for over 90 of cases. However, only
    10-20 of heavy smokers develop COPD, indicating
    individual susceptibility. The development of
    COPD is also related to the number of cigarettes
    smoked per day the risk of death from COPD in
    patients smoking 30 cigarettes daily is 20 times
    that of a non-smoker.
  • Climate and air pollution are of less importance
  • social class and occupation may also play a part
    in aetiology, but these effects are difficult to
    separate from that of smoking, indoor and outdoor
    air pollutants, and nutritional status.
  • Some animal studies suggest that diet could be a
    risk factor for COPD but this has not been
    proven in humans.

4
Pathophysiology
  • The most consistent pathological finding is
    hypertrophy and increase in number of the
    mucus-secreting goblet cells of the bronchial
    tree, evenly distributed throughout the lung but
    mainly seen in the larger bronchi.
  • In more advanced cases, the bronchi themselves
    are obviously inflamed and pus is seen in the
    lumen. Microscopically there is infiltration of
    the walls of the bronchi and bronchioles with
    acute and chronic inflammatory cells and lymphoid
    follicles in severe disease.

5
  • The epithelial layer may become ulcerated and,
    when the ulcers heal, squamous epithelium may
    replace the columnar cells.
  • The inflammation is followed by scarring and a
    remodelling process that thickens the walls and
    leads to widespread narrowing in the small
    airways.
  • The small airways are particularly affected early
    in the disease, initially without the development
    of any significant breathlessness. This initial
    inflammation of the small airways is reversible
    and accounts for the improvement in airway
    function if smoking is stopped early.

6
  • In later stages the inflammation continues, even
    if smoking is stopped.
  • The Lung Parenchyma developed emphysema which is
    characterized by destruction of gas-exchanging
    airspaces, i.e., the respiratory bronchioles,
    alveolar ducts, and alveoli. Their walls become
    perforated and later obliterated with coalescence
    of small distinct airspaces into abnormal and
    much larger airspaces.

7
  • a1-Antitrypsin deficiency
  • a1-Antitrypsin inhibitor is an antiproteinase
    inhibitor produced in the liver, secreted into
    the blood and which diffuses into the lung. Here
    it functions as an antiprotease that inhibits
    neutrophil elastase, a proteolytic enzyme capable
    of destroying alveolar wall connective tissue.
    More than 75 alleles of the a1-antitrypsin
    inhibitor gene have been described. The three
    main phenotypes are MM (normal), MZ (heterozygous
    deficiency) and ZZ (homozygous deficiency).
  • Hereditary deficiency of a1-antitrypsin inhibitor
    accounts for about 2 of emphysema cases. A small
    minority develop liver disease .

8
  • Emphysema is classified into distinct pathologic
    types
  • Centriacinar emphysema, the type most frequently
    associated with cigarette smoking, and it is most
    prominent in the upper lobes and superior
    segments of lower lobes and is often quite focal.
  • Panacinar emphysema ,is usually observed in
    patients with a1 AT deficiency, which has a
    predilection for the lower lobes.
  • N.B, smoking-related emphysema is usually mixed,
    particularly in advanced cases, and these
    pathologic classifications are not helpful in the
    care of patients with COPD.
  • Irregular emphysema,there is scarring and damage
    affecting the lung parenchyma patchily without
    particular regard for acinar structure.

9
Centrilobular
10
Panlobular
11
  • Emphysema leads to expiratory airflow limitation
    and air trapping. The loss of lung elastic recoil
    results in an increase in TLC while the loss of
    alveoli with emphysema results in decreased gas
    transfer.
  • Other mechanisms that have been suggested for
    airflow limitation are
  • Inflammation and scarring cause the small airways
    to narrow.
  • Mucus secretion which blocks the airways.
  • These all cause narrowing of the small airways
    and trapping of air leading to hyperinflation of
    the lungs and breathlessness.

12
Clinical Presentation
  • History
  • The three most common symptoms in COPD are cough,
    sputum production, and exertional dyspnea. 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.
  • As COPD advances, the principal feature is
    worsening dyspnea on exertion .
  • Accompanying worsening airflow obstruction is an
    increased frequency of exacerbations . Patients
    may also develop resting hypoxemia and require
    institution of supplemental oxygen.

13
Physical Findings
  • In the early stages of COPD, patients usually
    have an entirely normal physical examination.
  • In patients with more severe disease, the
    physical examination is notable for a prolonged
    expiratory phase and expiratory wheezing. In
    addition, signs of hyperinflation include a
    barrel chest.
  • Patients with severe airflow obstruction may also
    exhibit use of accessory muscles of respiration,
    sitting in the characteristic "tripod" position
    to facilitate the actions of the sterno-mastoid,
    scalene, and intercostal muscles. Patients may
    develop cyanosis, visible in the lips and nail
    beds.

14
  • Although traditional teaching is that patients
    with predominant emphysema, termed "pink
    puffers," are thin and non cyanotic at rest and
    have prominent use of accessory muscles, and
    patients with chronic bronchitis are more likely
    to be heavy and cyanotic ("blue bloaters"),
    current evidence demonstrates that most patients
    have elements of both bronchitis and emphysema
    and that the physical examination does not
    reliably differentiate the two entities.
  • Signs of overt right heart failure, termed cor
    pulmonale, are relatively infrequent since the
    advent of supplemental oxygen therapy.
  • N.B,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,
    because the development of lung cancer is the
    most likely explanation .

15
Complications
  • Respiratory failure
  • The later stages of COPD are characterized by the
    development of respiratory failure(type 2). For
    practical purposes this is said to occur when
    there is either a Pao2 of less than 8 kPa (60
    mmHg) or a Paco2 of more than 7 kPa (55 mmHg) .
  • Cor pulmonale The persistence of chronic
    alveolar hypoxia and hypercapnia leads to
    constriction of the pulmonary arterioles and
    subsequent pulmonary arterial hypertension.
    Cardiac output is normal or increased but salt
    and fluid retention occurs as a result of renal
    hypoxia leading to Cor pulmonale .

16
Investigations
  • Pulmonary 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 lt 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.

17
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18
  • 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. Occasionally Moraxella catarrhalis
    may cause infective exacerbations.
  • Electrocardiogram. In advanced cor pulmonale the
    P wave is taller (P pulmonale) and there may be
    right bundle branch block (rSR' complex) and the
    changes of right ventricular hypertrophy
  • Echocardiogram - performed to assess cardiac
    function.
  • a1-Antitrypsin levels. The normal range is 2-4
    g/L.

19
Global Initiative in Obstructive Lung Disease
(GOLD) criteria
Symptoms FEV () Stage of COPD
None 80 At risk 0
variable 80 mild 1
mild to moderate 50-79 moderate 11
limited exertion 30-49 sever 111
limited daily activities lt30 Very sever 1V
20
Management
  • Smoking cessation
  • Enforcing the patient to stop smoking is vital.
    Even at a late stage of the disease this may slow
    down the rate of deterioration and prolong the
    time before disability and death occur.
  • Drug therapy
  • This is used both for the short-term management
    of exacerbations and for the long-term relief of
    symptoms. In many cases the drugs used are
    similar to those used in asthma .
  • -Bronchodilators Many patients feel less
    breathless following the inhalation of a
    ß-adrenergic agonist such as salbutamol (200 µg
    every 4-6 hours).
  • -More prolonged and greater bronchodilatation is
    achieved with antimuscarinic agents ipratropium
    (40 µg four times daily) or oxitropium (200µg
    twice daily).

21
  • Objective evidence of improvement in the peak
    flow or FEV1 may be small and decisions to
    continue or stop therapy should be based on the
    patient's reported symptoms.
  • Long-acting preparations of theophylline are of
    little benefit.
  • In symptomatic patients with COPD, a trial of
    corticosteroids is always indicated, since a
    proportion of patients have a large, unsuspected,
    reversible element to their disease and airway
    function may improve considerably. Prednisolone
    30 mg daily should be given for 2 weeks, with
    measurements of lung function before and after
    the treatment period. If there is objective
    evidence of a substantial degree of improvement
    in airflow limitation (FEV1 increase gt 15),
    prednisolone should be discontinued and replaced
    by inhaled corticosteroids (beclometasone 400µg
    twice daily in the first instance, adjusted
    according to response). The long-term value of
    regular inhaled corticosteroids in all patients
    with COPD has not been proven.

22
  • Antibiotics Prompt antibiotic treatment
    shortens exacerbations and should always be given
    in acute episodes as it may prevent hospital
    admission and further lung damage. Long-term
    treatment with antibiotics remains controversial
  • Diuretic therapy This is necessary for all
    oedematous patients. Daily weights should be
    recorded during acute inpatient episodes.
  • a1-Antitrypsin replacement Weekly or monthly
    infusions of a1-antitrypsin have been recommended
    for patients with serum levels of this compound
    below 310 mg/L and abnormal lung function.
    Whether this modifies the long-term progression
    of the disease has still to be determined.
  • Vaccines Patients with COPD should receive
    yearly influenza vaccine. These patients should
    also receive one dose of the polyvalent
    pneumococcal polysaccharide vaccine (a single
    dose usually provides lifelong immunity).

23
  • Secondary polycythaemia - venesection is
    recommended if the PCV is gt 55.

24
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