Topic: COPD, Chronic Bronchitis, Emphysema Faculty: General Medicine Course: BSc ATOT - 2nd year

1. COPD
Dr. Salman Ansari
Kanachur Institute of Medical Sciences

2. Contents
● COPD
● Chronic Bronchitis
● Emphysema

4. ALVEOLI

5. COPD

6. Chronic obstructive pulmonary disease
Definition: It is a pulmonary disease characterized by
airflow limitation which is not fully reversible and is
progressive

7. Other names: chronic obstructive lung disease (COLD),
chronic obstructive airway disease (COAD), chronic airflow
limitation (CAL) and chronic obstructive respiratory disease
(CORD).

8. Diseases included under COPD:
- Emphysema
- Chronic bronchitis

9. Pathogenesis
● airflow limitation
● due to both small airway obstruction and emphysema
● Narrowed airways
● fibrosis

10. CHRONIC
BRONCHITIS

11. Chronic Bronchitis
Definition: Chronic productive cough for at least 3
months in 2 consecutive years
● It is a type of Chronic Obstructive Pulmonary
Disease(COPD)

12. Incidence
- Age: middle aged to late adult life
- Gender: males>females
- More common in smokers

13. Types of chronic bronchitis
(1) Simple chronic bronchitis
(2) chronic mucopurulent bronchitis
(3) chronic asthmatic bronchitis
(4) chronic obstructive bronchitis.

14. Risk factors
Environmental Host factors

15. Risk factors
Environmental
- Tobacco smoke
- Indoor air pollution
- Occupational dust
exposure(coal dust,
silica)
- Lung infections
Host factors

16. Risk factors
Environmental Host factors
- Genetic factors
- Hypersensitive
airway

17. Risk factors
Environmental
- Tobacco smoke
- Indoor air pollution
- Occupational dust
exposure(coal dust,
silica)
- Lung infections
Host factors
- Genetic factors
- Hypersensitive
airway

18. Causes
● Cigarette smoking 🚬
● Air pollution: SO2, NO2
● Occupational dust exposure(mining)
● Respiratory tract infections

19. Pathogenesis
Irritation by inhaled air pollutants
Excess mucus secretion
Hypertrophy of submucosal glands
and hyperplasia of goblet cells

20. Irritation by inhaled air pollutants
● Tobacco smoke
● Dust
● Cotton
● Sulfur dioxide
● Nitrogen dioxide
● Silica
Inflammation
of airways
Lymphocytes,
neutrophils

21. Excess mucus secretion
● Neutrophils → stimulate hypertrophy of submucosal
glands in large airways
● Increase in goblet cells in small airways → lead to
excess mucus production which blocks small airways

22. GOBLET GOBLET CELL

25. 1) Increase in size of
submucosal glands
2) Increase in number of
goblet cells
Increased mucus
production

26. Morphology
Gross:
● Thickening of mucus membranes
● Excessive mucus secretion

28. Microscopy:
● Chronic inflammation: many lymphocytes
● Increased size of submucosal glands(hypertrophy)
● More number of goblet cells(hyperplasia)

30. Clinical features
● Middle aged males,
heavy smokers
● Persistent cough with
sputum - since many
years
● Dyspnea on exertion -
shortness of breath
● Wheezing - noisy
breathing

32. Investigations
● Pulmonary function test(PFT):
● Reduced FEV 1 , FEV 1 /FVC (less than 0.7),
FVC, PEF
● Increased RV, FRC, TLC
● Chest X-ray: hyperinflation, bullae present
● High resolution CT scan(HRCT)
● Arterial blood gas(ABG)
● Hb: increased

33. Complications
● Carbon dioxide narcosis
● Respiratory failure
● Secondary polycythemia
● Cor pulmonale
● Pneumonia
● Tuberculosis
● Lung cancer

34. Treatment
General measures
- Regular exercises and management of nutrition
- Weight loss, if the patient is obese.
- Smoking cessation: Stop smoking completely
- Reduce smoke: Reducing the risk from indoor and
outdoor air pollution.

35. Drug therapy
- both for the short-term management of exacerbations and for
the long-term relief of symptoms
Bronchodilators: for breathlessness
- Short-acting β-agonist(SABA): salbutamol 200 µg or
terbutaline 500 µg 6 hourly
- Long-acting β-agonists(LABA): salmeterol 50 μg twice daily
or formoterol (12 μg powder inhaled twice daily)
- Antimuscarinic (anticholinergic) drugs: ipratropium bromide

36. - Corticosteroids: inhaled corticosteroid(ICS)
- Treatment of infections: azithromycin
- Prevention of infections: vaccination with polyvalent
pneumococcal and influenza vaccines
- Antimucolytic agents: bromhexine
- Chest physiotherapy
- Long-term oxygen therapy(LTOT)

37. Acute exacerbation of COPD
Definition: acute increase in symptoms of COPD above
the normal baseline of the patient
Causes: respiratory tract infections, air pollution
Infections by bacteria or viruses

38. Treatment
- Oxygen administration: saturation of 88-92%
through nasal cannula or face mask
- Bronchodilators: SABA(salbutamol 2.5 mg every
20 minutes for initial 1–2 hours) via nebulisation
with anticholinergic agent (ipratropium bromide 0.5
mg)

39. - Antibiotics:
- Outpatient: Doxycycline, cotrimoxazole or
amoxicillin–clavulanate can be given
- Hospitalized patients: Intravenous
antibiotics (azithromycin or fluroquinolone or
a third-generation cephalosporin-like
ceftriaxone or cefotaxime).
- Corticosteroids

40. Complications
● Long-standing chronic bronchitis → Cor
pulmonale(right sided heart failure)
● Respiratory failure
● pneumothorax

41. Emphysema

42. Emphysema
Definition: Irreversible dilation of air spaces distal to terminal
bronchiole, accompanied by destruction of their walls.

43. Types of emphysema
Classified according to anatomic distribution.
1. Centriacinar
2. Panacinar
3. Paraseptal
4. Irregular

44. Pathogenesis
Factors involved in pathogenesis of emphysema are:
● Inflammatory mediators released in lung
● Protease-antiprotease mechanism
● Imbalance of oxidants and antioxidants
● Oxidative stress
● Airway infection

45. Protease- antiprotease imbalance hypothesis:
- Injury due to heavy smoking and pollution causes
activation of inflammatory cells like neutrophils
- This causes damage to epithelial cells
- genetic deficiency of the antiprotease a1-
antitrypsin: enhanced tendency to develop
emphysema which is increased by smoking.

46. ● α1-Antitrypsin: present in serum, tissue fluids, and
macrophages
● Major inhibitor of proteases (particularly elastase)
secreted by neutrophils.
● Emphysema results from destructive effect of high
protease activity in people with low antiprotease activity.

47. Clinical features
● Dyspnea , cough, wheezing
● Prolonged expiration
● Barrel chest
● Pink puffers

50. Complications
(i) Cor pulmonale
(ii) congestive heart failure due to secondary pulmonary
hypertension and pneumothorax.
(iii) death

51. Death is due to:
● Respiratory acidosis and coma
● Rt sided heart failure
● Massive collapse secondary to pneumothorax

52. Investigations
- Chest X-ray: flat diaphragm, long and narrow heart
- CT chest
- Pulmonary function tests

54. Treatment
- No specific treatment
- Prevention of progression: Cessation of smoking and
avoidance of occupational exposure.
- Treatment of aggravating factors and complications:
Treatment of infections, respiratory failure and right
heart failure.
- Chest physiotherapy

55. - Surgical therapy: Ablation of giant bullae, lung volume
reduction surgery reduced hyperinflation of one or both
lungs and/or laser resection.
- Heart and lung transplantation: In young patients with
severe emphysema due to α 1 -antitrypsin deficiency

56. Questions
LE:
- what is COPD? describe briefly its pathophysiology and treatment
SE:
SA:
- RF of COPD
- pathophysiology of COPD
- drugs used in COPD
- diseases caused by smoking

57. For notes, click here
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References:
● Archith Boloor, Ramadas Nayak - Exam Preparatory
Manual for Undergraduates - Medicine
Questions:
salman.s.ansari92@gmail.com
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