Chronic obstructive pulmonary disease (COPD)

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Chronic obstructive pulmonary disease (COPD)
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• 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.

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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.

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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.

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• 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.

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• 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.

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• 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 .

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• 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.

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Centrilobular
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Panlobular
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• 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.

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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.

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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.

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• 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 .

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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 .

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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.

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• 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.

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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
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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).

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• 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.

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• 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).

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

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