These slides offer a comprehensive overview of Chronic Obstructive Pulmonary Disease (COPD), a progressive lung disorder characterized by airflow limitation and persistent respiratory symptoms. Delve into the pathophysiology of COPD, understanding the role of smoking, environmental factors, and genetic predisposition in its development. Learn about the clinical manifestations, including chronic bronchitis and emphysema, and how they contribute to the disease's progression. The presentation explores diagnostic methods such as spirometry and imaging techniques, as well as the GOLD guidelines that aid in disease staging and management. Discover the multifaceted treatment approaches, including bronchodilators, inhaled corticosteroids, pulmonary rehabilitation, and lifestyle modifications. These slides provide a comprehensive resource for grasping the complexities of COPD and its management.

1. COPD IN ELDERLY
DR SARAT HAZARIKA

2. DEFINITION
• Chronic obstructive pulmonary disease (COPD) is defined as a
disease state characterized by persistent respiratory symptoms and
airflow obstruction
• Emphysema is primarily a pathological diagnosis that affects the
air spaces distal to the terminal bronchiole. It is characterized by
abnormal permanent enlargement of lung air spaces with the
destruction of their walls without any fibrosis and destruction of
lung parenchyma with loss of elasticity.

3. • Chronic Bronchitis is defined as a chronic cough and sputum
production for at least 3 months a year for 2 consecutive years.

4. COPD PREVALENCE IN INDIA
• Prevalence of COPD from India (from different population-based
studies): highly variable
• The estimated national prevalence of COPD was 8.9%
• Rural areas had the highest prevalence of COPD, at 12.0% , which
was double that in urban communities 5.9%
• More common in males.
• Median male to female ratio: 1.6:1

5. RISK FACTORS
• Environmental factors
• Tobacco smoke: accounts for 95% of cases in the UK
• Indoor air pollution: cooking with biomass fuels in confined
areas in developing countries
• Occupational exposures, such as coal dust, silica and cadmium.
• Low birth weight: may reduce maximally attained lung function
in young adult life.

6. • Environmental factors contd..
• Lung growth
• Infections
• Low socioeconomic status
• Cannabis smoking
• Host factors
• Genetic Factors : α1-antitrypsin deficiency
• Airway hyper-reactivity

7. PATHOPHYSIOLOGY
• COPD has both pulmonary and systemic components.
• The presence of airflow limitation combined with premature airway
closure leads to gas trapping and Hyperinflation.
• Enlargement of mucus-secreting glands and Increase in number of
goblet cells, accompanied by an inflammatory cell infiltrate, result
in increased sputum production leading to chronic bronchitis

8. • Pulmonary hyperinflation also results, which flattens the
diaphragmatic muscles and leads to an increasingly horizontal
alignment of the intercostal muscles, placing the respiratory
muscles at a mechanical disadvantage. The work of breathing is
therefore markedly increased.

9. PATHOPHYSIOLOGY : PULMONARY COMPONENT

10. PATHOPHYSIOLOGY : SYSTEMIC COMPONENT

11. PATHOLOGY
• Emphysema : Classified by the
pattern of the enlarged
airspaces:
• Centriacinar,
• Panacinar and
• Paraseptal
• Irregular
• Bullae form in some individuals.
• This results in impaired gas
exchange and respiratory failure.

12. CLINICAL FEATURES
• The three most common symptoms in COPD are cough, sputum
pro- duction, and exertional dyspnea.
• Haemoptysis may complicate exacerbations of COPD but should
not be attributed to COPD without thorough investigation.
• Breathlessness usually prompts presentation to a health
professional. The level should be quantified : MRC dyspnoea scale
may be used
• In advanced disease : Oedema and morning headaches (which
may suggest hypercapnia).

13. CLINICAL FEATURES CONTD.
• Two classical phenotypes have been described:
• Pink puffers : Typically thin and breathless, and maintain a normal
PaCO2 until the late stage of disease
• Blue bloaters : Develop (or tolerate) hypercapnia earlier and may
develop oedema and secondary polycythaemia.
• In practice, these phenotypes often overlap.

14. MODIFIED MEDICAL RESEARCH COUNCIL (MRC)
DYSPNOEA SCALE
• Grade Degree of breathlessness related to activities
• 0 No breathlessness, except with strenuous exercise
• 1 Breathlessness when hurrying on the level or walking up a
slight hill
• 2 Walks slower than contemporaries on level ground because
of. breathlessness or has to stop for breath when walking
at own pace
• 3 Stops for breath after walking about 100 m or after a few
minutes on level ground
• 4 Too breathless to leave the house, or breathless when dressing

15. INVESTIGATIONS
• Chest X-ray B : Dark Lung Fields,
Tubular Heart, Hyperinflation changes,
increased rib count.
• Pulmonary Function Tests : The
diagnosis requires objective
demonstration of airflow obstruction
by spirometry and is established when
the post- bronchodilator FEV1/FVC is <
70%. The severity of COPD may be
defined in relation to the post-
bronchodilator FEV1.

16. • HRCT THORAX
• In Chronic bronchitis, bronchial wall thickening , enlarged
vessels. Broncho vascular irregularity and fibrosis.
• Emphysema, Alveolar septal destruction and airspace
airspace enlargement, Centrilobular emphysema is predominantly
seen in the upper lobes with panacinar emphysema
predominating in the lower lobes. Paraseptal emphysema tends to
occur near lung fissures and pleura. Formation of
giant bullae may lead to compression of mediastinal structures,
while rupture of pleural blebs may produce
spontaneous pneumothorax/pneumomediastinum

17. INVESTIGATIONS
• Others-
• St George’s Respiratory Questionnaire (SGRQ).
• COPD Assessment Test
• COPD Control Questionnaire

18. ASSESSMENT OF SEVERITY

19. MANAGEMENT
• The management of COPD focuses on improving breathlessness, reducing the
frequency and severity of exacerbations, and improving health status and
prognosis.
• Reducing exposure to noxious particles and gases
• Bronchodilators
• Combined inhaled glucocorticoids and bronchodilators
• Oral glucocorticoids

20. MANAGEMENT CONTD.
• Pulmonary rehabilitation
• Oxygen therapy
• Surgical intervention
• Surgical intervention

21. ACUTE EXACERBATIONS OF COPD
• Characterised by an increase in symptoms and deterioration in lung function and
health status.
• More frequent as the disease progresses
• Usually triggered by bacteria, viruses or a change in air quality.
• May be accompanied by the development of respiratory failure and/or fluid
retention and represent an important cause of death.

22. ACUTE EXACERBATIONS OF COPD
• Many patients can be managed at home with the use of increased bronchodilator
therapy, a short course of oral glucocorticoids and, if appropriate, antibiotics.
• The presence of cyanosis, peripheral oedema or an alteration in consciousness
should prompt referral to hospital.
• In other patients, consideration of comorbidity and social circumstances may
influence decisions regarding hospital admission.

23. TREATMENT OF AECOPD
• Oxygen therapy
• Bronchodilators : Nebulised short-acting β2-agonists combined with an
anticholinergic agent (e.g. salbutamol and ipratropium) should be administered.
• Glucocorticoids
• Antibiotic therapy
• Non Invasive Ventilation.