2. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)
Collective term for an inflammatory
lung disease in which airway
obstruction is progressive and only
partially reversible by bronchodilators
RISK factors include
• tobacco smoking,
• environmental chemical exposures
(biomass fuel, air pollution, etc.),
• genetic abnormalities,
• abnormal lung development,
• alpha1 –antitrypsin and
• accelerated aging
3. • COPD = Chronic bronchitis +
Emphysema
• Chronic bronchitis: is a chronic
inflammation of the lower respiratory tract
characterized by excessive mucous secretion,
cough, & dyspnea associated with recurrent
infections of the lower respiratory tract
• Chronic Bronchitis: persistent cough with
sputum production for > 3months/year for 2
years
4. EMPHYSEMA
• A complex lung disease characterized
by damage to the gas- exchanging
surfaces of the lungs (alveoli)
• permanent enlargement of air spaces
distal to the terminal bronchiole due to
alveolar septal destruction
• Lung Parenchyma
• Emphysema affects the structures
distal to the terminal bronchiole,
consisting of the respiratory bronchiole,
alveolar ducts, alveolar sacs, and
alveoli, known collectively as the acinus
5. Subtype of emphysema
• Centrilobular emphysema (Proximal acinar)
• Abnormal dilation or destruction of the respiratory
bronchiole, the central portion of the acinus. It is
commonly associated with cigarette smoking,
6. • Panacinar emphysema
• Refers to enlargement or
destruction of all parts of the
acinus
• Seen in alpha-1 antitrypsin
deficiency and in smokers
• Paraseptal emphysema
• Distal acinar - the alveolar ducts
are predominantly affected.
7. EPIDEMIOLOGY
• Chronic obstructive pulmonary disease (COPD)
affects about 300 million people worldwide,
resulting in approximately 64 million disability-
adjusted life years.
• The prevalence of COPD was estimated to be 7.6%
8. PATHOPHYSIOLOGY
1. Abnormal inflammatory response of the lungs due to
toxic gases.
2. Response occurs in the airways parenchyma &
pulmonary vasculature.
3. Narrowing of the airway takes place
4. Destruction of parenchyma leads to emphysema
5. Destruction of lung parenchyma leads to an imbalance
of proteinases/ant proteinases. (this proteinases
inhibitors prevents the destructive process)
6. Pulmonary vascular changes Thickening of vessels
Collagen deposit Destruction of capillary beds.
7. Mucus hypersecretion(cilia dysfunction, airflow limitation,
cor pulmonale (RVF)
1. Hypertrophy and hyperplasia of mucous glands and goblet cells
8. Chronic cough and sputum production
10. ETIOLOGY
•Tobacco Smoking (90% of cases)
•Air Pollution : PROLONG EXPOSURE to
Coal, wood, dust chemicals
•Genetics : Alpha-1 Antitrypsin(AAT)
deficiency
• AAT protein protects the lung from ENZYMES
released during inflammation
11.
12. • Chronic cough
• Sputum
production
• Dyspnea on
exertion
• Dyspnea at rest
• Weight loss
• Barrel chest
13.
14.
15. DIAGNOSIS
• Pulmonary function studies are used to
help confirm the diagnosis of COPD,
determine disease severity, and follow
disease progression.
• Spirometry
• Arterial blood gas (ABGs) measurements
may also be obtained to assess baseline
oxygenation and gas exchange
• Chest x-ray; CT scan
• alpha1antitrypsin deficiency screening
16.
17.
18. X-RAY
• BRONCHITIS
• No apparent abnormality
• Or thickened and increased lung markings
are noted
• EMPHYSEMA
• Marked over inflation is noted with flattend
and low diaphragm
• Intercostal space becomes widen
• A horizontal pattern of ribs
• A long thin heart shadow
• Decreased markings of lung peripheral
vessels
19. •CT
• Greater sensitivity and specificity for emphysema
• For evaluation of bullous disease
• Blood examination
• In exacerbation or acute infection in airway, leukocytosis may
be detected.
• Sputum examination
• Streptococcus pneumonia
• haemophilus influenzae
• moraxella catarrhalis
• Klebsiella pneumonia
20. • Arterial blood gas measurements (in hospital)
• PaO2 < 8.0 kPa with or without PaCO2 > 6.7 kPa when
breathing room air indicates respiratory failure.
21. TREATMENTS
• SMOKING CESSATION
• Bronchodilators:
• Relieve bronchospasm and reduce airway obstruction by
allowing increased oxygen distribution throughout the lungs
and improving alveolar ventilation
• B2 agonists
• Short acting – salbutamol & terbutaline
• Long acting – salmeterol & formoterol
• Anti-cholinergic agents - Tiotropium
• Theophylline
22. • Glucocorticoids
• Regular treatment with inhaled glucocorticoids is appropriate for
symptomatic patients with an FEV1<50% pred and repeated
exacerbations
• Chronic treatment with systemic glucocorticoids should be avoided
because of an unfavorable benefit-to-risk ratio
• COMBINATION THERAPY
• Combination therapy of long acting B2-agonists and inhaled
corticosteroids show a significant additional effect on pulmonary
function and a reduction in symptoms
• Mainly in patients with an FEV1<50%pred
23. • Corticosteroids. Inhaled and systemic
corticosteroids (oral or intravenous) may also be used in
COPD but are used more frequently in asthma.
• Although it has been shown that corticosteroids do not
slow the decline in lung function, these medications
may improve symptoms.
• Other Medications including Patients should receive a
yearly influenza vaccine and the pneumococcal
vaccine every 5 to 7 years as preventive measures.
24. MANAGEMENT OF EXACERBATION
• An exacerbation of COPD is difficult to diagnose, but signs and
symptoms may include increased dyspnea, increased sputum
production and purulence, respiratory failure, changes in mental
status, or worsening blood gas abnormalities.
• Primary causes for an acute exacerbation include
tracheobronchial infection and air pollution.
25. Oxygen Therapy
• Oxygen 15h/day
• Oxygen therapy can be administered as long- term continuous
therapy, during exercise, or to prevent acute dyspnea.
• Long-term oxygen therapy has been shown to improve the
patient's quality of life and survival.
• GOAL – SaO2 >90%
• PaO2 >60mmHg at sea level and rest
26. SURGICAL MANAGEMENT
• Bullectomy-bullae are enlarged airspaces that do not contribute
to ventilation but occupy space in the thorax, these areas may
be surgically excised
• lung volume reduction surgery it
• Involves the removal of a portion of the diseased lung
parenchyma. This allows the functional tissue to expand.
• lung transplantation
27.
28. 67 Year old Male with Shortness Of Breath
with exertion
• complains of progressively worsening shortness of breath with
exertion over the last year
• He currently smokes half a pack of cigarettes daily and has
accumulated 45 pack years.
• He uses a short acting beta agonist 3-4 times a day with limited
relief. He is no longer able to ride a bike with his grandchildren
• last hospitalization was 4 months ago secondary to right lower lobe
pneumonia.
• He does not complain of weight loss or loss of appetite.
• He has a past medical history of dietary controlled diabetes and mild
osteoarthritis.
• Medications include Albuterol and Celecoxib.
29. • On exam respiratory rate is 22 per minute;
• chest exam reveals mild end expiratory wheezing without use of
accessory muscles of respiration and no retractions.
• No clubbing, cyanosis or lower extremity edema is noted.
• Spirometry reveals an FVC of 78% predicted, FEV1 of 62%
predicted and FEV1/FVC of 68%, post bronchodilator.
30. Based on GOLD guidelines your patient:
• FEV1 is between 50-80% of predicted the patient has moderate
COPD
31. Based on GOLD guidelines the most
appropriate next step would be to initiate:
• Our patient has moderate COPD based on an FEV1/FVC ratio
less than 70% and an FEV1 between 50-80%
• GOLD guidelines recommend the use of a long acting
bronchodilator for patients with moderate COPD.
• A long acting cholinergic such as tiotropium should be
considered in our patient
• An inhaled corticosteroid may be indicated in patients with
severe or very severe disease in combination with a long acting
bronchodilator.
32. T he patient develops a cough productive of
green thick sputum associated with
increasing shortness of breath, a low grade
fever, and a clear chest x-ray
• Infection is the most common cause of exacerbation
• The most frequent bacterial organisms identified during an
exacerbation are Haemophiles influenzae, Moraxella
catarrhalis, and Streptococcus pneumonia and empiric antibiotic
therapy should be directed accordingly
33. KEY POINTS
• Chronic obstructive pulmonary disease (COPD) is a chronic
inflammatory lung disease that causes obstructed airflow from the
lungs.
• Chronic obstructive pulmonary disease (COPD) is responsible for
one death every four minutes in the US.
• COPD is under recognized and undertreated. GOLD
recommendations facilitate establishing a diagnosis and determining
appropriate therapy.
• Spirometry should be performed at presentation and periodically.
• Obstruction is determined by the presence of an FEV1/FVC ratio of
less than 70%
• Severity of COPD is then based on the FEV1 as mentioned above
• Judicious use of empiric antibiotics should be considered in
exacerbations associated with increase or change in color of sputum
especially when accompanied by worsening symptoms
