IT IS A CHROMIC OBSTRUCTIVE PULODISORDER TAHY AFFECTS AIRWAYS

2. INTRODUCTION
 Chronic Obstructive Pulmonary Disease (COPD) is a preventable
and treatable disease with some significant extrapulmonary
effects that may contribute to the severity in individual patients.
 Its pulmonary component is characterized by airflow limitation that
is not fully reversible.
 The airflow limitation is usually progressive and associated with
an abnormal inflammatory response of the lung to noxious
particles or gases.
 The chronic airflow limitation characteristic ofCOPD is caused by
a mixture of small airway disease (obstructive bronchitis) and
parenchyma destruction (emphysema),

3. EPIDEMIOLOGY
• 14 million people in the United States have COPD.
• COPD is now the fourth leading cause of death in
the United States, and it is the only common
cause of death that is increasing in incidence.
• The World Health Organization predicts that by
2020 COPD will rise from its current ranking as
the 12th most prevalent disease worldwide to the
5th and from the 6th most common cause of
death to the 3rd.

4. STAGES OF COPD
• Stage I: Mild FEV1/FVC < 0.70
FEV1 ^ 80% predicted
• Stage II: Moderate FEV1/FVC < 0.70
50% ] FEV1 < 80% predicted
• Stage III: Severe FEV1/FVC < 0.70
30% < FEV1 < 50% predicted
• Stage IV: Very Severe FEV1/FVC < 0.70
FEV1 < 30% predicted or FEV1 <
50% predicted plus chronic respiratory

6. PATHOPHYSIOLOGY
• COPD is characterized by chronic inflammatory
changes that lead to destructive changes and
development of chronic airflow limitation.
• The processes that has been proposed to play a
major role in the pathogenesis of COPD include
inflammatory changes, oxidative stresses and
imbalance between aggressive and protective
defense system in lungs

7. • The stimulus for activation of inflammatory cells and
mediators is an exposure to noxious particles and
gases through inhalation
• The inflammation of COPD is referred to as
neutrophilc in nature but macrophages and CD8+
lymphocytes also play a major roles
• The inflammatory cells release a variety of chemical
mediators, of which tumor necrosing factor alpha,
interleukin 8 and leukotrene B4 play major roles

8. Oxidative stresses
• An altered interaction between oxidants and antioxidants
present in airways is responsible for increased oxidative
stress present in copd
• The increased oxidants generated by cigarrate smoke react
with and damage various proteins and lipids, leading to tissue
and cell damage
• Oxidants also promote inflammation directly and exacerbate
the protease anti protease imbalance by inhibiting
antiprotease activity
• In smokers in whom COPD develops, the production of
antiproteases may be inadequate to neutralize the effects of
multiple proteases

9. In chronic obstructive pulmonary
disease the balance appears to be
tipped in favor of increased
proteolysis, because of either an
increase in proteases, including
neutrophil elastase, cathepsins,
and matrix metalloproteinases, or a
deficiency of antiproteases, which
may include (alpha)1-antitrypsin,
elafin, secretory leukoprotease
inhibitor, and tissue inhibitors of
matrix metalloproteinases

11. • Pathologic changes of COPD affect large and
small airways, lung parenchyma and pulmonary
vasculature
• Parenchymal changes – affect alveoli and
pulmonary capillaries
• Vascular change- thickening of pulmonary blood
vessel which further lead to increased pulmonary
pressure
• Mucus secretions increased and ciliary movement
is impaired

12. Cor -pulmonale
• The consequence of long standing COPD and chronic hypoxia
is secondary pulmonary hypertension which can lead to cor-
pulmonale or right sided heart failure
• In response to chronic hypoxia there will be vasoconstriction
and vascular remodeling leading to elevated pulmonary artery
pressure
• F it is sustained cor-pulmonale can develop characterized by
hypertrophy of right ventricle n response to increased
pulmonary vascular resistance

13. Asthma and COPD

14. MANAGEMENT OF COPD
• An effective COPD management plan includes four
components:
(1) Assess and Monitor Disease;
(2) Reduce Risk Factors;
(3) Manage Stable COPD
(4) Manage Exacerbations.
• These goals should be reached with minimal side
effects from treatment, a particular challenge in COPD
patients because they commonly have comorbidities

15. COMPONENT 1: ASSESS AND MONITOR DISEASE
• A clinical diagnosis of COPD should be considered in
any patient who has dypsnea, chronic cough or sputum
production, and/or a history of exposure to risk factors
for the disease.
• For the diagnosis and assessment of COPD, spirometry
is the gold standard as it is the most reproducible,
standardized, and objective way of measuring airflow
limitation.
• The presence of a post bronchodilator FEV1/FVC < 0.70
and FEV1 < 80% predicted confirms the presence of
airflow limitation that is not fully reversible.

16. • Assessment of COPD severity is based on the patients
level of symptoms, the severity of the spirometric
abnormality, and the presence of complications.
• Measurement of arterial blood gas tensions should be
considered in all patients with FEV1 < 50% predicted or
clinical signs suggestive of respiratory failure or right heart
failure.
• COPD is usually a progressive disease and lung function
can be expected to worsen over time, symptoms and
objective measures of airflow limitation should be
monitored to determine when to modify therapy and to
identify any complications that may develop
• Comorbidities are common in COPD and should be actively
identified.

17. COMPONENT 2: REDUCE RISK FACTORS
• Smoking cessation is the single most effective—and
cost effective—intervention in most people to reduce
the risk of developing COPD and stop its
progression (Evidence A).
• Reduction of total personal exposure to tobacco
smoke, occupational dusts and chemicals, and
indoor and outdoor air pollutants are important goals
to prevent the onset and progression of COPD.

18. SMOKING CESSATION
• Quitting smoking can prevent or delay the development of airflow
limitation, or reduce its progression and can have a substantial
effect on subsequent mortality.
• Effective interventions include nicotine replacement with transdermal
patches, gums, and nasal sprays; counseling from physicians and
other health professionals (with or without nicotine replacement
therapy); self-help and group programs; and community-based stop-
smoking challenges.
Counseling delivered by physicians and other health professionals
significantly increases quit rates over self-initiated strategies. Even a
brief (3-minute) period of counseling to urge a smoker to quit results in
smoking cessation rates of 5-10%.

19. OCCUPATIONAL EXPOSURES
• In the United States, it has been estimated that up to 19% of COPD
in smokers and up to 31% of COPD in nonsmokers may be
attributable to occupational dust and fume exposure, and the
burden may be higher in countries where there is higher exposure
to inhaled particles, fumes and gases.
• Many occupations have been shown to be associated with
increased risk of developing COPD, particularly those that involve
exposure to fumes and mineral and biological dusts.
• The main emphasis should be on primary prevention, which is best
achieved by the elimination or reduction of exposures to various
substances in the workplace. Secondary prevention, achieved
through surveillance and early case detection,

20. INDOOR AND OUTDOOR AIR POLLUTION
• Reducing the risk from indoor and outdoor air
pollution is feasible and requires a
combination of public policy and protective
steps taken by individual patients.
• Reduction of exposure to smoke from biomass
fuel, particularly among women and children,
is a crucial goal to reduce the prevalence of
COPD worldwide.

21. COMPONENT 3: MANAGE STABLE COPD
• The overall approach to managing stable COPD
should be individualized to address symptoms
and improve quality of life.
• The three aspects of management of COPD are
Patient education
 Pharmacological treatment
 Non pharmacological treatment

22. EDUCATION
• For patients with COPD, health education plays an important role in
smoking cessation (Evidence A) and can also play a role in improving skills,
ability to cope with illness and health status.
• The topics that seem most appropriate for an education program include:
smoking cessation;
basic information about COPD and path physiology of the
disease;
 general approach to therapy and specific aspects of medical
treatment
 self-management skills;
strategies to help minimize dyspnea;
 advice about when to seek help;
self-management and decision-making during exacerbations;
advance directives and end-of-life issues

23. PHARMACOLOGIC TREATMENT
• Pharmacologic therapy is used to prevent and control symptoms,
reduce the frequency and severity of exacerbations, improve health
status, and improve exercise tolerance.
• None of the existing medications for COPD have been shown to
modify the long-term decline in lung function that is the hallmark of
this disease
• Treatment tends to be cumulative with more medications being
required as the disease state worsens.
• Regular treatment needs to be maintained at the same level for
long periods of time unless significant side effects occur or the
disease worsens.

24. Bronchodilators
• Bronchodilator medications are central to the symptomatic management
of COPD(Evidence A)
• They are given either on an as-needed basis for relief of persistent or
worsening symptoms, or on a regular basis to prevent or reduce
symptoms.
• COPD patients tend to be older than asthma patients and more likely to
have comorbidities, so their risk of developing side effects is greater.
• When treatment is given by the inhaled route, attention to effective drug
delivery and training in inhaler technique is essential.
• Although monotherapy with long-acting 2-agonists appears to be safe
combining bronchodilators with different mechanisms and durations of
action may increase the degree of bronchodilaton for equivalent or lesser
side effects.
• Regular treatment with long-acting bronchodilators is more effective and
convenient than treatment with short acting bronchodilators. (Evidence A)

25. β2-agonists.
• Oral therapy is slower in onset and has more side effects than inhaled
treatment(Evidence A)
• The bronchodilator effects of short-acting 2-agonists usually wear off
within 4 to 6 hours(Evidence A).
• Long-acting inhaled 2-agonists, such as salmeterol and formoterol, show a
duration of effect of 12 hours or more with no loss of effectiveness
overnight or with regular use in COPD patients129-132 (Evidence A).
• Adverse effects
 resting sinus tachycardia whch has the potential to precipitate cardiac
rhythm disturbances
 Exaggerated somatic tremor
 hypokalemia can occur, especially when treatment is combined with
thiazide diuretics.

26. Anticholinergic medications
• The most important effect of anticholinergic medications, such as
ipratropium, oxitropium and tiotropium bromide, in COPD patients
appears to be blockage of acetylcholinees effect on M3 receptors
• The long acting anticholinergic tiotropium has a pharmacokinetic
selectivity for the M3 and M1 receptors.
• The bronchodilating effect of short-acting inhaled anticholinergics
lasts longer than that of short-acting 2-agonists, with some
bronchodilator effect generally apparent up to 8 hours after
administration
• Tiotropium has a duration of action of more than 24 hours
• Adverse effects. Anticholinergic drugs are poorly absorbed The main
side effect is dryness of the mouth.

27. Methyl xanthines
• Theophylline is effective in COPD but, due to its potential toxicity,
inhaled bronchodilators are preferred when available.
• Low dose theophylline reduces exacerbations in patients with COPD
but does not increase post-bronchodilator lung function(Evidence
B).
• Problems include the development of atrial and ventricular
arrhythmias (which can prove fatal) and grand mal convulsions
(which can occur irrespective of prior epileptic history). More
common and less dramatic side effects include headaches,
insomnia, nausea, and heartburn, and these may occur within the
therapeutic range of serum theophylline.
• Clearance of the drug declines with age.

28. Glucocorticosteroids
• Regular treatment with inhaled glucocorticosteroids
does not modify the longer decline of FEV1 in patients
with COPD.
• However, regular treatment with inhaled glucocorticos-
teroids has been shown to reduce the frequency of
exacerbations and thus improve health status for
symptomatic COPD patients with an FEV1 < 50%
predicted(Stage III: Severe COPD and Stage IV: Very
Severe COPD) and repeated exacerbations (for
example, 3 in the last 3 years)(Evidence A

29. • Oral glucocorticosteroids: short-term. there
appears to be insufficient evidence to
recommend a therapeutic trial with oral
glucocorticosteroids in patients with Stage II:
Moderate COPD, Stage III: Severe COPD, or Stage
IV: Very Severe COPD
• long-term treatment with oral
glucocorticosteroids is not recommendedin COPD
(Evidence A).

30. Influenza vaccines
• Influenza vaccines can reduce serious illness and death
in COPD patients by about 50% (Evidence A).
• Vaccines containing killed or live, inactivated viruses
are recommended as they are more effective in elderly
patients with COPD
• In addition, this vaccine has been shown to reduce the
incidence of community-acquired pneumonia in COPD
patients younger than age 65with an FEV1 < 40%
predicted180 (Evidence B).

31. Alpha-1 antitrypsin augmentation therapy
• Young patients with severe hereditary alpha-1
antitrypsin deficiency and established
emphysema may be candidates for alpha-
1antitrypsin augmentation therapy.
• However, this therapy is very expensive, is not
available in most countries, and is not
recommended for patients with COPD that is
unrelated to alpha-1 antitrypsin deficiency
(Evidence C).

32. Antibiotics
• There is no current evidence that the use of
antibiotics, other than for treating infectious
exacerbations of COPD and other bacterial
infections, is helpful (Evidence A).
• There is no evidence that prophylactic
antibiotics prevent acute exacerbations.

33. Mucolytic agents
• Eg (ambroxol, erdosteine, carbocysteine,
iodinated glycerol).
• The regular use of mucolytics in COPD has been
evaluated in a number of long-term studies with
controversial results
• Although a few patients with viscous sputum
may benefit from mucolytics the overall benefits
seem to be very small, and the widespread use of
these agents cannot be recommended at present
(Evidence D).

34. Antioxidant agents
• Eg N-acetylcysteine,
• A large randomized controlled trial found no
effect of N-acetylcysteine on the frequency of
exacerbations, except in patients not treated
with inhaled glucocorticosteroids.

35. Immunoregulators
• Studies using an immunoregulator in COPD
show a decrease in the severity and frequency
of exacerbations.
• However, additional studies to examine the
long-term effects of this therapy are required
before its regular use can be recommended.

36. Narcotics (morphine)
• Oral and parenteral opioids are effective for
treating dyspnea in COPD patients with advanced
disease
• Others
- Nedocromil and leukotriene modifiers have not
been adequately tested in COPD patients and
cannot be recommended. There was no evidence
of benefit -and some evidence of harm
(malignancy and pneumonia)- from an anti-TNF-
alpha antibody (infliximab) tested in moderate to
severe COPD

37. NON-PHARMACOLOGIC TREATMENT
• Rehabilitation
• The principal goals of pulmonary rehabilitation are to
reduce symptoms, improve quality of life, and increase
physical and emotional participation in everyday
activities.
• The three components of rehablitation are
Exercise training
Nutrition counseling
Education.

38. Oxgyen
• Oxygen therapy, one of the principal nonpharmacologic treatments for patients
with Stage IV: Very Severe COPD
• can be administered in three ways: longer continuous therapy, during exercise,
and to relieve acute dyspnea.
• The primary goal of oxygen therapy is to increase the baseline PaO2 to at least
8.0 kPa (60 mmHg) at sea level and rest, and/or produce an SaO2 atleast 90%,
which will preserve vital organ function by ensuring adequate delivery of oxygen.
• The long-term administration of oxygen (> 15 hours perday) to patients with
chronic respiratory failure has been shown to increase survival
• It can also have a beneficial impact on hemodynamics, hematologi
ccharacteristics, exercise capacity, lung mechanics, and mental state
• Cost considerations.
Supplemental home oxygen is usually the most costly component of outpatient
therapy for adults with COPD who require this therapy

39. Surgical Treatments
• Bullectomy.
Bullectomy is an older surgical procedure for
bullous emphysema. In carefully selected
patients, this procedure is effective in
reducing dyspnea and improving lung function
(Evidence C).

40. Lung volume reduction surgery (LVRS)
• LVRS is a surgical procedure in which parts of
the lung are resected to reduce hyperinflation,
making respiratory muscles more effective
pressure generators by improving their
mechanical efficiency
• LVRS is an expensive palliative surgical
procedure and can be recommended only in
carefully selected patients.

41. Lung transplantation
• Criteria for referral for lung transplantation
include FEV1 < 35% predicted,PaO2 < 7.3-8.0
kPa (55-60 mm Hg), PaCO2 > 6.7 kPa(50 mm
Hg), and secondary pulmonary hypertension
• Lung transplantation is limited by the shortage
of donor, complications and cost

42. COMPONENT 4: MANAGE EXACERBATIONS
• An exacerbation of COPD is defined as an event in the natural course of
the disease characterized by a change in the patients baseline
dyspnea,cough, and/or sputum that is beyond normal day-to-day
variations, is acute in onset, and may warrant a change in regular
medication in a patient with underlying COPD.
• The most common causes of an exacerbation are infection of the tracheo
bronchial tree and air pollution, but the cause of about one-third of
severe exacerbations cannot be identified(Evidence B)
Exacerbations affect the quality of life and prognosis of patients with
COPD.
Hospital mortality of patients admitted for a hyperbaric COPD
exacerbation is approximately10%, and the long-term outcome is poor.

43. Controlled oxygen therapy
• Oxygen therapy is the cornerstone of hospital
treatment of COPD exacerbations.
• Supplemental oxygen should be titrated to
improve the patientes hypoxemia.
• Once oxygen is started, arterial blood gases
should be checked 30-60 minutes later to ensure
satisfactory oxygenation without CO2 retention
or acidosis.

44. Bronchodilator therapy
• Short-acting inhaled 2-agonistsare usually the preferred
bronchodilators for treatment of exacerbations of COPD(Evidence
A).
• If a prompt response to these drugs does not occur, the addition
of an anticholinergic is recommended
• Despite its widespread clinical use, the role of methylxanthines
in the treatment of exacerbations of COPD remains controversial.
Methylxanthines ( theophylline or aminohylline) are currently
considered second-line intravenous therapy, used when there is
inadequate or insufficient response to short-acting
bronchodilators(Evidence B)
• There are no clinical studies that have evaluated the use of
inhaled long-acting bronchodilators (either 2-agonists or
anticholinergics) with or without inhaled glucocorticosteroids
during an acute exacerbation.

45. Glucocorticosteroids
 Oral or intravenous glucocorticosteroids are
recommended as an addition to other therapies in
the hospital management of exacerbations of COPD
(Evidence A).
 Thirty to 40 mg of oral prednisolone daily for 7-10
days is effective and safe (Evidence C).
 Prolonged treatment does not result in greater
efficacy and increases the risk of side effects (e.g.,
hyperglycemia, muscle atrophy).

46. Antibiotics
• Patients with exacerbations of COPD with the following
three cardinal symptoms: increased dyspnea, increased
sputum volume, and increased sputum purulence
. Patients with exacerbations of COPD with two of the
cardinal symptoms, if increased purulence of sputumis
one of the two symptoms
• Patients with a severe exacerbation of COPD
thatrequires mechanical ventilation (invasive or
noninvasive

47. Respiratory Stimulants.
• Respiratory stimulants are not recommended for
acute respiratory failure.
• Doxapram,a nonspecific but relatively safe respiratory
stimulant available in some countries as an intravenous
formulation, should be used only when noninvasive
intermittent ventilation is not available or not
recommended.

49. CONCLUSION
• The previous view of COPD as untreatable
should now be replaced by a positive
approach to management with several
measures that improve the quality of life in
patients with symptomatic disease.
• Smoking cessation is of the utmost
importance