2. DEFINITION
Global initiative for chronic obstructive lung
diseases defines COPD as:
“Disease characterized by airflow limitation
that is not fully reversible, usually progressive
and associated with abnormal inflammatory
response of the lungs to noxious particles or
gases.”
Common conditions associated with COPD are:
• Chronic bronchitis
• Emphysema
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3. CHRONIC BRONCHITIS:
Chronic bronchitis is associated with chronic or
recurrent excessive mucus secretion in to the
bronchial tree with cough that is present on most
days for at least 2 consecutive years in a patient, in
whom other causes of chronic cough have been
excluded.
EMPHYSEMA:
Abnormal permanent enlargement of airspaces
distal to the terminal bronchioles accompanied by
destruction of their walls without obvious fibrosis.
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4. EPIDEMIOLOGY
It is the 6th leading cause of death in the world.
Mortality rate is higher in males than females, and
in whites than blacks.
COPD is the 2nd leading cause of disability in the
united states.
In India prevalence rate indicates that about 5%
male and 2.7% female over the age of 30 suffer
from COPD.
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5. RISK FACTORS
Major risk factor for COPD development is a
history of cigarette smoking.
Environmental factors Host factors
•Tobacco smoke
•Occupational exposure
•Air pollution
•Serious respiratory disease
•Recurrent broncho-
pulmonary infection.
•Genetic predisposition
(α1- antitrypsin)
•Airway hyper-
responsiveness
•Impaired lung growth
•Gender
•Age
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6. PATHOGENESIS
Exposure to noxious chemical & gases – ↑sed
bronchial reactivity – inflammation
Chronic inflammation - remodeling & narrowing of
airway lumen- fixed / irriversible airflow
obstruction
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7. Four areas of lungs are affected:
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Central airways
• Inflammatory
exudates - ↑sed
number & size of
goblet cells &
mucus glands –
mucus
hypersecretion
• Airway cilia
destroyed - ↓sed
clearance of
mucus.
Peripheral
airways
• Thickenin
g of
smooth
muscles
&
connectiv
e tissues.
Lung
parenchyma
• Air spaces
enlarged,
attachmen
ts lost –
alveolar
collapse.
Pulmonary
vasculature
• Thickenin
g of
pulmonar
y vessels
9. Balance in antiprotease (protective) and
protease (aggressive) activity in the lungs is
disturbed in COPD – injury and damage to
normal lung tissue.
Noxious chemicals and gases increases
oxidative stress – stimulate inflammatory cells
to release additional proteases.
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10. PATHOPHYSIOLOGY
Pathologic changes in COPD are exhibited as:
Air flow limitation
Reduced ratio of FEV1 to FVC
Increased functional residual capacity due to air
trapping and thoracic hyper inflation.
Mucus plugging, chronic airflow limitation and
thoracic hyper inflation disturb normal ventilatory
dynamics.
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11. 6/29/2016 11
• Abnormality of gas
exchange: Changes in
pulmonary vasculature
• Pulmonary hypertension:
Elevated mean
pulmonary artery
pressure and pulmonary
vascular resistance
• Hypertrophy of right
ventricle: Development
of cor pulmonale.
Consequences
of advanced
disease
12. Mucus plugging – colonization of
bacteria – contribute to chronic
inflammation.
Factors contributes to airflow
obstruction.
Increased mucus
Airway wall fibrosis
Alveolar collapse
Normal elastic recoil of lung
during exhalation is lost in COPD-
patient use abdominal and chest
muscle to force air out- further
collapse of airways & air trapping
– thoracic hyper inflation6/29/2016 12
13. EXACERBATION
A change in patient’s baseline symptoms
(dyspnoea, cough, sputum production) beyond
day to day variability sufficient to warrant a
change in management.
Eosinophils are prominent during
exacerbation.
Typically have an infectious etiology, either
bacterial or viral.
‘haemophylus influenzae’, ‘streptococcus
pneumoniae’, ‘moraxella catarrhalis’ etc are
responsible for most of bacterial respiratory
infections.6/29/2016 13
14. CLINICAL PRESENTATION
SYMPTOMS
Cough
Sputum production
Dyspnea
PHYSICAL EXAMINATION
Cyanosis of mucosal membrane
Barrel chest
Increased resting respiratory rate
Shallow breathing
Pursed lips during expiration
Use of accessory respiratory
muscles
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15. DIAGNOSTIC TEST RESULTS:-
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• Post bronchodilator FEV1/FVC < 70% -
COPD.
Spirometry
• Identifies thoracic hyper inflation, barrel
chest, and increased bronchovascular
markings.
Chest X-ray
• To exclude asthma if there is a doubt about
diagnosis.
Serial domiciliary peak
flow measurements
• Particularly with early onset disease or a
minimal smoking/family history
α1-Antitrypsin
• To identify organism if persistantly present
and purulent .
Sputum culture
• To reveal right ventricular hypertrophy and
changes consistent with cor pulmonale
ECG
16. Severity classification of COPD
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Severity stage Classification Predicted FEV1
1 Mild ≥80%
2 Moderate ≥50% & <80%
3 Severe ≥30% & < 50%
4 Very severe <30% or < 50%
with respiratory
failure
17. TREATMENT
Treatment objectives endorsed by GOLD:
Prevent disease progression
Relieve symptoms and improve exercise tolerance
Improve health status
Prevent and treat exacerbations
Reduce mortality
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18. THERAPEUTIC PLAN
1. Approaches to treatment
a) Pharmacotherapy
b) Non pharmacologic approach
c) Surgical management
d) Managing exacerbations
2. Improving outcomes
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19. a) PHARMACOTHERAPY
International guidelines recommend a stepwise
approach to pharmacotherapy based on disease
severity.
Patients with intermittent symptoms- treated with
short acting bronchodilators
Persistent symptoms – initiate long acting
bronchodilators
Patient with FEV1 < 50%, with frequent exacerbation
– inhaled corticosteroids
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20. In pharmacotherapy, inhaled route of
administration is preferred because it is more
efficacious and safer than available oral
therapies.
Inhaled therapy can be delivered by metered
dose inhaler (MDI), Dry powder inhaler (DPI) or a
nebulizer
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21. Continue previous therapies; initiate therapeutic trial with inhaled corticosteroids at
moderate – high dose.
Continue previous therapies. Initiate therapeutic trial of oral SR theophylline, titrate
to 8/12 mcg/ml
Symptoms persists, patient experiences frequent exacerbations .
If not previously done initiate and titrate inhaled anti cholinergics to 6 puffs QID
Combination
:scheduled long
acting inhaled β2
agonist & PRN short
acting inhaled β2
agonist
Combination: scheduled
short acting inhaled β2
agonist +inhaled
anticholinergic& continue
PRN short acting inhaled
β2 agonist
Combination: scheduled long
acting inhaled β2 agonist +
inhaled anticholinergic &
continue PRN short acting
inhaled β2 agonist.
Change initial therapy to scheduled basis and continue / initiate PRN inhaled β2
agonist
Initiate therapy with PRN short acting inhaled β2 agonist/ PRN inhaled
anticholinergic.
Patient with intermittent symptoms of COPD
22. I. BRONCHODILATORS
Bronchodilators used for treating COPD includes:-
Short and Long acting inhaled β2 agonist
Short and Long acting inhaled anticholinergics
Methylxanthines
i. ANTICHOLINERGICS
Ipratropium bromide
Tiotropium bromide
MOA
blocks Ach – ↓ses cyclic GMP – privent bronchial
smooth muscle contraction.
Reduce sputum volume.6/29/2016 22
23. 6/29/2016 23
Ipratropium
Initial MDI dosing – 40μg (2 inhalations)
QID
Dosing can be ↑sed to – 4 inhalations
QID
Administered through MDI with or
without spacer
Ipratropium bromide solution: dosing
500μg /2.5mL or more via nebulizer QID.
It has a slower onset of action, and effect
last for about 4-6 hours.
Patient complaints
Dry mouth
Nausea
Occasional metallic taste
Tiotropium
• It should be administered once
daily only via a handihaler
device , which delivers 10 μg of
tiotropium.
• Patient should not be placed
on both ipratropium and
tiotropium due to increased
risk of anticholinergic side
effects.
• It has a slower onset of action
within 30 minutes, with a peak
effect in 3 hours and persists
for about 24 hours
24. ii. β 2 AGONISTS
Indication
Used as first line bronchodilator or in conjunction
with anticholinergic agents in the maintenance
treatment of COPD.
Mechanism
Stimulate adenelyl cyclase – increased formation
of cyclic AMP – bronchial smooth muscle
relaxation.
Increases mucociliary clearance by increasing
ciliary activity.
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25. Administration and dosage
Normally administered via inhalation (DPI,MDI
with or without spacer, nebulizer) , if the
patient is unable to use inhalational devices
properly, oral agent is used cautiously
Agents with same duration of action should not
be used in combination.
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27. Long acting agents
• Available dosage forms :
4.5, 12 μg MDI & DPI
• Duration of action: 12
hours
Salmeterol
• Available dosage forms :
25, 50 μg MDI & DPI
• Duration of action: 12 hoursFormoterol
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28. iii.METHYLXANTHINES
THEOPHYLLINE
Theophylline compounds added to the drug regimen after
an unsuccessful trial of ipratropium bromide and β
adrenergics.
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• Inhibition of phosphodiesterase –
increase cyclic AMP level
• Inhibition of calcium influx in to smooth
muscle.
• Prostaglandin antagonism
• Stimulation of endogenous
catecholamines
• Adenosine receptor antagonism
• Inhibition of release of mediators from
mast cells and leukocytes
Mechanism
of action
It produce
bronchodilatio
n through:-
29. It also Increases
– mucociliary clearance
– stimulate respiratory drive
– enhance diaphragmatic contractility
– Improves ventricular ejection fraction
– stimulate renal diuresis.
ADMINISTRATION AND DOSAGE
It is available as 100 – 600mg pills, having variable
duration of action up to 24 hours.
a trial of 1-2 months with serum concentration
maintained at 5-12μg/mL and maximized.
Sustained release oral preparations are
appropriate for long term management of COPD.
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30. iv. CORTICOSTEROIDS
INDICATION:
Systemic corticosteroids: oral – for acute COPD
exacerbations
Inhaled corticosteroids: given alone and in
combination with long acting β2 agonist.
Mechanism of action
Reduce capillary permeability – reduce mucus.
Inhibit release of proteolytic enzymes from
leukocytes
Inhibit prostaglandins
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31. Agents used:
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systemic
• Prednisone: available as 5 – 60mg pills
• Methyl prednisolone: available as 4, 8 ,16 mg
pills
Inhaled
• Beclomethasone:50-400μg (MDI & DPI), 0.2-0.4 mg/ml
(solution for inhalation)
• Budesonide: 100, 200, 400μg (DPI), 0.20, 0.25, 0.5 mg/ml
soln for inhalation
• Fluticasone: 50-500μg (MDI & DPI)
Combinati
on with
long
acting β2
agonist
• Formoterol/beclometasone: 6/100 μg(MDI)
• Formoterol/budesonide: 4.5/160 μg (MDI), 9/320μg (DPI)
• Formoterol/mometasone:10/200, 10/400 μg (MDI)
• Salmeterol/Fluticasone: 50/100, 250, 500 μg(DPI)
32. Long term adverse effect:
Osteoporosis
Muscular atrophy
Thinning of skin
Development of cataracts
Adrenal suppression.
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33. v. α1 ANTITRYPSIN REPLACEMENT THERAPY
Used as an augmentation therapy in patient
with inherited AAT deficiency.
To maintain the serum concentrations above
the protective threshold.
Consists of weekly infusion of pooled human
AAT to maintain AAT plasma level greater than
10 micromolars.
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34. vi. ANTIBIOTICS
Indication: Used to treat exacerbation with
suspected infections.
Agents used for therapy include:
2nd generation cephalosporins : cefuroxime, cefaclor
Clotrimoxazole : trimethoprim + sulfamethoxazole
β lactam with or without β lactamase inhibitor :
amoxicillin, amoxicillin – clavulanate
Macrolides : azithromycin
Ketolides : telithromycin
Oral fluoroquinolone : ciprofloxacin, gatifloxacin
COPD exacerbations are treated for 3 – 10 days,
depending on the agent used and the patient.6/29/2016 34
35. vii.PHOSPHODIESTERASE 4 INHIBITORS
The principal action of phosphodiesterase-4
inhibitors is to reduce inflammation by inhibiting
the breakdown of intracellular cyclic AMP.
Roflumilast
It is a once daily oral medication with no direct
bronchodilator activity, although it has been
shown to improve FEV1in patients treated with
salmeterol or tiotropium.
Dose: Roflumilast - 500 mcg (Pill)
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36. Adverse effects.
Phosphodiesterase-4 inhibitors have more
adverse effects than inhaled medications for
COPD
The most frequent adverse effects are
nausea,
reduced appetite,
abdominal pain,
diarrhea,
sleep disturbances
headache
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37. 6/29/2016 37
MUCOLYTICS
• Improve sputum
clearance and
disrupt mucus plugs
• Eg :- Iodinated
glycerol
EXPECTORANTS
• Guaifenesin may
be used
ANTIOXIDANTS
• N- acetyl cysteine
may reduce
exacerbation
frequency
38. b) NON PHARMACOLOGICAL THERAPY
1. TOBACCO CESSATION STRATEGIES.
The 5 ‘A’ system is commonly used to evaluate
and assist smokers.
1. ASK : Use systematic approach to identify
tobacco users
2. ADVICE : Urge all tobacco users to quit
3. ASSESS : Determine willingness to make a
cessation attempt
4. ASSIST : Provide support for quit smoking
5. ARRANGE : Schedule follow up and monitor.
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39. Drugs for smoking cessation.
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AGENT USUAL DOSE DURATION COMMON
COMPLAINTS
Bupropion SR 150 mg OD- oral 12 weeks – 6
months
Insomnia, dry
mouth
Nicotine gum 2-4 mg gum
PRN
12 weeks Sore mouth,
dyspepsia
Nicotine inhaler 6-16 catridges
/day
Up to 6 months Sore mouth,
sore throat
Nicotine nasal
spray
8-40 doses / day 3 – 6 months Nasal irritation
Nicotine
patches
7 – 21 mg every
24 hours
Up to 8 weeks Skin reaction,
insomnia
40. 2. PULMONARY REHABILITATION
Pulmonary rehabilitation program includes
Patient education
Exercise training
Psychological support
Nutritional therapy
Along with smoking cessation & optimal medical
treatment
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41. For the lungs to get more air
PURSED-LIP BREATHING
(like breathing out slowly into a
straw)
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INHALE EXHALE
42. 6/29/2016 42
Sit comfortably
&
relax your shoulders
Put one hand on your
abdomen. Now inhale
slowly through your
nose. (Push your
abdomen out while you
breathe in)
Then push in your
abdominal muscles
and breathe out using
the pursed-lip
technique
For the lungs to get more air
DIAPHRAGMATIC BREATHING
43. 3. IMMUNIZATIONS
Annual influenza vaccination is recommended by
american thoracic society
GOLD guidelines recommend pneumococcal
vaccine for all COPD patient with age 65 years
and older.
4. OXYGEN THERAPY
Commonly used in two situations
Acute exacerbation of COPD with drop in Pa O2 <
55mmHg.
Patients who are chronically hypoxemic.
Goal: correct arterial hypoxemia and prevent
secondary organ damage.6/29/2016 43
44. 5. CHEST PHYSIOTHERAPY.
Loosens secretions, helps re expand the lungs,
increases efficacy of respiratory muscle use.
Techniques used:-
Deep breathing
Coughing
Postural drainage
Chest percussion and vibration
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45. c) 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 – reduce obstruction – improve
functional lung volume
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46. 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
Lung transplantation is an option in severe
emphysema and other options have failed.
Usually one lung is transplanted because the
survival rate has proved to be higher for people
with single-lung transplants than for people with
double-lung transplants6/29/2016 46
47. d) MANAGING EXACERBATIONS
General management of exacerbation include:
Supplemental oxygen therapy
Intensification of bronchodilator regimen
Systemic corticosteroid therapy
Antimicrobial therapy
Ventilator support
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48. 6/29/2016 48
LEVEL 1
• Treated with
intensification of
bronchodilator therapy
– dosage of short acting
bronchodilator is
increased
• Administered either by
MDI or nebulizer
• Treatment also include
the use of systemic
corticosteroids
(prednisone )
LEVEL 2
• Treated on
an inpatient
basis,
treatment is
similar to
that of level
1
exacerbation
s
LEVEL 3
• Require
ventilator
support.
• Aggressive
bronchodilator
therapy is used
• Corticosteroid
therapy and
broad spectrum
antimicrobial
therapy may
used.
49. 2. IMPROVING OUTCOMES
i. PATIENT EDUCATION
Counseling can help the patient to develop self
management skills, improve coping abilities and
improve overall health status.
For inhalation therapies, the patient must
understand how to use the various delivery
devices correctly.
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