This document summarizes COPD (chronic obstructive pulmonary disease). It defines COPD as a disease characterized by irreversible airflow limitation. COPD includes emphysema, chronic bronchitis, and small airways disease. The major risk factor is cigarette smoking. The pathology involves changes in the large airways, small airways (<2mm), and lung parenchyma. Emphysema is classified as centriacinar or panacinar. Treatment focuses on smoking cessation, bronchodilators, inhaled corticosteroids, lung volume reduction surgery, lung transplantation, and managing exacerbations.

1. COPD
PRESENTED BY: DR SHUBHAM SHARMA
PG RESIDENT
DEPT. OF MEDICINE
JMC JHALAWAR

2. COPD
• Chronic obstructive pulmonary disease (COPD) is defined as a
disease state characterized by airflow limitation that is not fully
reversible
COPD includes :
1. emphysema, an anatomically defined condition characterized by
destruction and enlargement of the lung alveoli;
2. chronic bronchitis, a clinically defined condition with chronic cough
and phlegm; and
3. small airways disease, a condition in which small bronchioles are
narrowed.
• COPD is present only if chronic airflow obstruction occurs; chronic
bronchitis without chronic airflow obstruction is not included
within COPD.

7. EMPHYSEMATOUS BULLAE

8. PATHOLOGY
• Cigarette smoke exposure may affect the large airways, small
airways(≤2 mm diameter), and alveoli.
• Changes in large airways cause cough and sputum, while
• changes in small airways and alveoli are responsiblefor
physiologic alterations.
• Emphysema and small airway pathology are both present in
most persons with COPD;

9. LARGE AIRWAY
• Cigarette smoking often results in mucus gland enlargement
and goblet cell hyperplasia, leading to cough and mucus
production that define chronic bronchitis, but these
abnormalities are not related to airflow limitation.
• Goblet cells not only increase in number but in extent through
the bronchial tree.
• Bronchi also undergo squamous metaplasia, predisposing to
carcinogenesis and disrupting mucociliary clearance.

10. SMALL AIRWAYS
• The major site of increased resistance in most individuals with
COPD is in airways ≤2 mm diameter.
• Characteristic cellular changes include goblet cell metaplasia,
with these mucus-secreting cells replacing surfactant-
secreting Clara cells.
• Smooth-muscle hypertrophy mayalso be present. These
abnormalities may cause luminal narrowing by fibrosis, excess
mucus, edema, and cellular infiltration.
• Reduced surfactant may increase surface tension at the air-
tissue interface, predisposing to airway narrowing or collapse.

11. LUNG PARENCHYMA
• Emphysema is characterized by destruction of gas-exchanging
air spaces, i.e., the respiratory bronchioles, alveolar ducts,
and alveoli.
• Their walls become perforated and later obliterated with
coalescence of small distinct air spaces into abnormal and
much larger air spaces.
• Macrophages accumulate in respiratory bronchioles of
essentially all young smokers.

12. EMPHYSEMA
• Emphysema is classified into distinct pathologic types, the
most important being centriacinar and panacinar.
• Centriacinar emphysema,
the type most frequently associated with cigarette smoking, is
characterized by enlarged air spaces found (initially) in
association with respiratory bronchioles.
• Centriacinar emphysema
is usually most prominent in the upper lobes and superior
segments of lower lobes and is often quite focal.

13. • Panacinar emphysema refers to abnormally
large air spaces evenly distributed within and
across acinar units.
Panacinar emphysema is usually observed in
patients with α1AT deficiency,
which has a predilection for the lower lobes.

14. PATHOPHYSIOLOGY
• AIRFLOW OBSTRUCTION
• HYPERINFLATION
• GAS EXCHANGE

15. RISK FACTORS
• CIGARRETE SMOKING
• RESPIRATORY INFECTIONS
• AMBIENT AIR POLLUTION
• OCCUATIONAL EXPOSURE
• PASSIVE OR SECOND HAND SMOKING
• GENETIC; ALPHA 1 A.T DEFICIENCY
• OTHERS

16. HISTORY
• The three most common symptoms in COPD are cough,
sputum production,and exertional dyspnea.
• Many patients have such symptoms 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.

17. • The development of exertional dyspnea, often
described as increased effort to breathe,
heaviness, air hunger, or gasping, can be
insidious.
• It is best elicited by a careful history focused
on typical physical activities and how the
patient’s ability to perform them has changed.

18. PHYSICAL FINDINGS
• odor of smoke or nicotine staining of fingernails.
• A prolonged expiratory phase and may include
expiratory wheezing.
• barrel chest and enlarged lung volumes with poor
diaphragmatic excursion as assessed by
percussion.
• Patients with severe airflow obstruction may also
exhibit use of accessorymuscles of respiration,
sitting in the characteristic “tripod”
• Patients may develop cyanosis,

19. • Although traditional teaching is that patients with
predominant
emphysema, termed “pink puffers,” are thin and
noncyanotic 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.

20. • Advanced disease may be accompanied by
cachexia, with significant
weight loss, bitemporal wasting, and diffuse loss
of subcutaneous adipose
tissue.

21. The degree of airflow obstruction is an
important prognostic factor in COPD
and is the basis for the Global Initiative for Lung
Disease (GOLD) severity classification

22. GOLD STAGING OF COPD

23. TREATMENT
STABLE PHASE COPD
Only three interventions—
1. smoking cessation,
2. oxygen therapy in chronically hypoxemic patients, and
3. lung volume reduction surgery in selected patients
with emphysema—
have been demonstrated
to influence the natural history of patients with COPD.
There is currently suggestive, but not definitive, evidence
that the use of inhaled glucocorticoids may alter
mortality rate (but not lung function).

24. PHARMACOTHERAPY
SMOKING CESSATION:
There are three principal pharmacologic
approaches to the problem:
1. bupropion; nicotine replacement therapy
available as gum, transdermal
2. patch, lozenge, inhaler, and nasal spray; and
3. varenicline, a nicotinic acid receptor
agonist/antagonist.

25. Current recommendations are that all adult,
nonpregnant smokers considering quitting be
offered pharmacotherapy, in the absence of
any contraindication to treatment.

26. • BRONCHODILATORS
• bronchodilators are used for symptomatic
benefit in patients with COPD.
• The inhaled route is preferred

27. • ANTICHOLINERGIC AGENTS
• Ipratropium bromide improves symptoms
• and produces acute improvement in FEV1.
Tiotropium, a long-acting V1 anticholinergic,
has been shown to improve symptoms and
reduce exacerbations
• a trial of inhaled anticholinergics is
recommended in symptomatic patients with
COPD

28. • BETA 2 AGONIST
• Long-acting inhaled ß agonists, such as
salmeterol or formoterol, have benefits
comparable to ipratropium bromide.
• Their use is more convenient than short-acting
agents.
• The addition of a ß agonist to inhaled
anticholinergic therapy has been
demonstrated to provide incremental benefit.

29. • INHALED GLUCOCORTICOIDS:
• Available data suggest that inhaled
glucocorticoids reduce exacerbation frequency
by ~25%.
• Their use has been associated with increased
rates of oropharyngeal candidiasis and an
increased rate and loss of bone density
.

30. • A trial of inhaled glucocorticoids should be
considered :
1. in patients with frequent exacerbations,
defined as two or more per year, and
2. in patients who demonstrate a significant
amount of acute reversibility in response to
inhaled bronchodilators
• ORAL STEROIDS: CHRONIC USE not
recommended

31. • THEOPHYLLINE: produces modest
improvements in expiratory flow rates and
vital capacity and a slight improvement in
arterial oxygen and carbon dioxide levels in
patients with moderate to severe COPD
• Monitoring of blood theophylline levels is
typically required to minimize toxicity.
• Roflumilast

32. • ANTIBIOTICS
• azithromycin, chosen for both its anti-
inflammatory and antimicrobial properties,
administered daily to subjects with a history
of exacerbation in the past 6 months
demonstrated a reduced exacerbation
frequency and longer time to first
exacerbation

33. NON PHARMACOLOGICAL TREATMENT
• General Medical Care
Patients with COPD should receive the influenza
vaccine annually
• LUNG VOLUME REDUCTION SURGERY:
Patient are excluded if they have
• significant pleural disease,
• a pulmonary artery systolic pressure >45
mmHg,
• extreme deconditioning,
• congestive heart failure, or other severe
comorbid conditions.

34. • Patients with an FEV1 <20% of predicted and
• either diffusely distributed emphysema on CT
scan or
diffusing capacity of lung for carbon monoxide
(DlCO) <20% of predicted have an increased
mortality rate after the procedure and thus are
not candidates for LVRS.

35. LUNG TRANSPLANTATION
Figure 314-4 Chest computed tomography scan of a patient with chronic obstructive pulmonary
disease who underwent a left single-lung transplant. Note the reduced parenchymal markings in
the right lung (left side of figure) as compared to the left lung, representing emphysematous
destruction of the lung, and mediastinal shift to the left, indicative of hyperinflation.

36. • COPD is currently the second leading indication for
lung transplantation (Fig. 314-4).
• Current recommendations are that candidates for lung
transplantation should have :
1. severe disability despite maximal medical therapy and
2. be free of comorbid conditions such as liver, renal, or
cardiac disease.
• In contrast to LVRS, the anatomic distribution of
emphysema and the presence of pulmonary
hypertension are not contraindications to lung
transplantation.

37. EXACERBATIONS OF COPD
• Exacerbations are episodes of increased dyspnea and
cough and change in the amount and character of
sputum.
• They may or may not be accompanied by other signs of
illness, including fever, myalgias, and sore throat.
• The frequency of exacerbations increases as airflow
obstruction increases.
• However, some individuals with very severe airflow
obstruction do not have frequent exacerbations;
• The history of prior exacerbations is a strong predictor
of future exacerbations

38. • Recently, an elevated ratio of the diameter of
the pulmonary artery to aorta on chest CT has
been associated with increased risk of COPD
exacerbations.
• Precipitating Causes and Strategies to Reduce
Frequency of Exacerbations
1. Bacterial infection/superinfection-- over 50%
of exacerbations.
2. Viral respiratory infections --- one-third of
COPD exacerbations.
3. In a significant minority of instances (20–
35%), no specific precipitant can be
identified.

39. • Chronic oral glucocorticoids are not
recommended for this purpose.
• Inhaled glucocorticoids reduce the frequency of
exacerbations by 25–30% in most analyses...
• The use of inhaled glucocorticoids should be
considered in patients with frequent
exacerbations or those who have an asthmatic
component, i.e., significant reversibility on
pulmonary function testing or marked
symptomatic improvement after inhaled
bronchodilators

40. • Similar magnitudes of reduction have been
reported for anticholinergic and long-acting β-
agonist therapy.
• The influenza vaccine has been shown to
reduce exacerbation rates in patients with
COPD.
• As outlined above, daily azithromycin
administered to subjects with COPD and an
exacerbation history reduces exacerbation
frequency

41. PATIENT ASSESSMENT IN A/E COPD
• The history should include quantification of the
degree of dyspnea by asking about
breathlessness during activities of daily living and
typical activities for the patient.
• The patient should be asked about fever;change
in character of sputum; any ill contacts; and
associated symptoms such as nausea, vomiting,
diarrhea, myalgias, and chills.

42. • The physical examination should incorporate
an assessment of the degree of distress of the
patient.
Specific attention should be focused on
1. tachycardia,
2. tachypnea,
3. use of accessory muscles,
4. signs of perioral or peripheral cyanosis,
5. the ability to speak in complete sentences,
and
6. the patient’s mental status.
.

43. The chest examination should establish the
1. presence or absence of focal findings,
2. degree of air movement,
3. presence or absence of wheezing,
4. asymmetry in the chest examination (suggesting
large airway obstruction or pneumothorax
mimicking an exacerbation), and
5. the presence or absence of paradoxical motion
of the abdominal wall

44. • Approximately 25% of x-rays in this clinical situation will be
abnormal, with the most frequent findings being pneumonia and
congestive heart failure.
• Patients with advanced COPD, those with a history of
hypercarbia, those with mental status changes
(confusion,sleepiness), or those in significant distress should
have an arterial blood-gas measurement.
• The presence of hypercarbia, defined as a Pco2 >45 mmHg,
has important implications for treatment

45. TREATMENT OF ACUTE
EXACERBATIONS
• BRONCHODILATORS
• ANTIBIOTICS
• GLUCOCORTECOIDS: The GOLD guidelines recommend 30–
40 mg of oral prednisolone or its equivalent for a period
of10–14 days.
• SUPPLIMENTAL OXYGEN
MECHANICAL VENTILATION: The initiation of noninvasive
positive
Pressure ventilation (NIPPV) in patients with respiratory
failure,defined as PaCO2 >45 mmHg, results in a significant
reduction in mortality rate, need for intubation, complications
of therapy, and hospital length of stay.

46. • Invasive (conventional) mechanical ventilation
via an endotracheal tube is indicated for
patients with severe respiratory distress
despite initial therapy, life-threatening
hypoxemia, severe hypercarbia and/or
acidosis, markedly impaired mental status,
respiratory arrest, hemodynamic instability, or
other complications