Asma Dan COPD

COPD
Chronic Obstructive Pulmonary

Disease
Definition
Chronic obstructive pulmonary disease (COPD)
is characterised by airflow obstruction. The
airflow obstruction is usually progressive,
not fully reversible and does not change
markedly over several months. 1
The disease is predominantly caused by smoking.
1. NICE 2004
The Umbrella Disease
Umbrella Disease
 COPD now preferred term for previous
diagnosis of bronchitis or emphysema,
chronic asthma
 Significant airflow obstruction may be

present before individual is aware of it
 May also be related to occupational

exposures e.g. asbestos
Characteristic
 Changes characteristic of the disease include:
 smooth muscle contraction (bronchoconstriction)
 mucus hypersecretion
 ciliary dysfunction
 pulmonary hyperinflation
 gas exchange abnormalities
 pulmonary hypertension
 cor pulmonale
 These abnormalities contribute to the characteristic
symptoms of COPD - chronic cough, sputum production
and dyspnoea 1
1 Pauwels et al, 2001

Asthma Is A Disease Of The Large
& COPD The Small Airways
Asthma Bronchitis
trachea
Emphysema Bronchitis
bronchi
alveoli
Healthy Respiratory Mucosa
This electron micrograph shows the
respiratory mucosa in a healthy
state
The cells are fully ciliated
The cilia beat in a co-ordinated

fashion to move mucus out of the
airways (mucociliary transport)
Scanning electron micrograph showing a sheet of

mucus being moved along by the cilia
Damaged Respiratory Mucosa
 Damage to the cilia and
epithelium occur as a result of
disease processes in COPD. This
can also occur as a result of
bacterial damage
 This slide shows the result of

bacterial infection stripping
away the cilia from the mucosa
 The damage to the cilia means

they are less effective in
removing mucus from the
airways
Scanning electron micrograph showing cilial and

epithelial damage induced by bacteria
Chronic Bronchitis
– ↑ in mucus glands and goblet cells
– Production of sputum on most days for > 3
months on 2 consecutive years
Small airway disease
(structural changes in the small airways
2-5mm)
> 50% of bronchioles may be effected before
any SOB
–↑ airway smooth muscle
– Inflammatory infiltration resulting in
structural narrowing and distortion
Collagen deposition / fibrosis / mucous plugging
Emphysema
•Dilation of alveolar wall
•↓ alveolar capillary network, loss of guy rope effect
•↓ lung tissue elasticity
•Caused by smoking » irritation » inflammation » neutrophils and
macrophages » release neutrophil elastase (type of proteases)
Normal Lung Emphysema

The COPD Patient
 Generally over 40 years 1
 A smoker or ex-smoker
 Presentation with:
 cough
 excessive sputum production
 shortness of breath
 Dyspnoea is the reason most

patients seek medical
attention 3
1. BTS, 1997; 3. GOLD, 2003

Diagnosis
 >35 years
 Smoker or ex-smoker
 Spirometry (obstructive pattern)
 Any symptoms :
 Exertional breathlessness
 Chronic cough
 Regular sputum production
 Frequent “winter bronchitis”
 Wheeze
 + no clinical features of asthma
Clinical features
of Asthma vs. COPD
Assessment of Severity of COPD
Severity of airflow FEV1 % predicted 1
obstruction
Mild 50-80%
Moderate 30-49%
Severe <30%
GOLD state that spirometry is the gold standard for diagnosing COPD,
severity is measured by FEV1.
1 NICE Guidelines 2004
Spirometry - The Sixth Vital
Sign
Indications: Symptoms or >10 pack year smoker
Impact of Chronic Disease
 Impairment
 Disability
 Handicap
COPD Therapy
Prolong Life Symptomatic
 Smoking Cessation  MDI Therapy

 Oxygen  SA beta-2 agonists
 Reduce exacerbations  LA beta-2 agonists
 SA and LA
 Pulmonary Anticholinergics
Rehabilitation
 Theophylline
 LVRS (selected patients)
 Corticosteroids
 Lung Transplantation (inhaled or oral)
 Combination
Preparations
 SABA and anticholinergic
 LABA and corticosteroids
Management of COPD (Stable)
 Use short acting bronchodilator PRN (beta2-

agonist or anti-cholinergic)
 If still symptomatic try combined therapy with
a short acting beta2 agonist and a short acting
anti-cholinergic.
 If still symptomatic use a long acting bronch-
dilator (beta2 agonist or anti-cholinergic)
Management
In moderate or severe COPD
 If still symptomatic consider a trial of a combination of a long acting beta2
agonist and inhaled corticosteroid. (Discontinue if no benefit after 4 – 6 weeks)
 If still symptomatic consider adding theophylline.
 Offer pulmonary rehab to all patients who consider themselves functionally

disabled (usually MRC 3 and above)
 Consider referral for surgery.
 End of Life Care (need to start these conversations ,what the future will hold,
discuss issues, worries and concerns with patients at an earlier stage. Palliative
care being part of end of life care)
Acute exacerbation of COPD
 Sustained worsening of patients symptoms from their usual
stable state, which is beyond normal day-to-day variations
and is acute in onset. 1
 Symptoms :
 Increased shortness of breath
 Increased sputum production and/or change in colour
 Increased cough
 Increased wheeze/tightness
 Decreased exercise tolerance
 Increased fatigue
 Confusion
1 NICE Guidelines 2004

COPD Exacerbation
Pathophysiology - Current Hypothesis
Chronic Inflammation
Viral Unknown
Infection 20%
25%
Bacterial Air
Infection Pollution
50% Acute 5%
Inflammation
Exacerbation
Natural History
Oxygen Therapy
 Long Term Oxygen
Therapy (LTOT)
 Short Burst Oxygen

Therapy
 Ambulatory Oxygen
Therapy
Benefits of LTOT
 Improved survival
 Prevention of deterioration of pulmonary haemodynamics
 Reduction in secondary polycythaemia
 Neuropsychological benefit
 improved sleep quality
 Increased renal blood flow
 reduction in cardiac arrhythmias
 Reduction in dyspnoea, improved exercise tolerance
 Should be worn for 15 hrs or more a day to gain these

benefits
Short Burst Oxygen Therapy
 Further research is required

 Episodic dyspnoea not relieved by other
treatments
 Palliative therapy or in emergency situations
 If improvement in dyspnoea or exercise
tolerance can be documented
Ambulatory Oxygen Therapy
 Improved exercise tolerance

 Reduced dyspnoea
 Improved quality of life
Medicines Management
 Flu and Pneumonia vaccination
 Bronchodilators
 Coticosteroids
 Mucolytics
Pharmacotherapy does not modify long-term decline, but is used to

–prevent and control symptoms / improve exercise tolerance
–reduce the frequency and severity of exacerbations
–improve health status
Long – Acting Inhaled bronchodilators e.g. Salmeterol /
Tiotropium
 Significant improvement in lung function 1-3
 better sustained improvement in lung function over 12 hours than

ipratropium bromide 1
 Improve shortness of breath day and night 1,3
 Reduce risk of exacerbations vs. placebo 1
 Clinically significant improvements in quality of life 4,5

 unlike ipratropium bromide, Salmeterol significantly increased the
percentage of patients showing a clinically relevant improvement in
health status compared with placebo 5
1. Mahler et al, 1999, 2. Mahler et al, 2001, 3. Boyd et al, 1997, 4. Jones et al, 1997, 5. Cox et al, 2000
Xanthines - e.g. theophylline
Less commonly used than other bronchodilators
 Only modest bronchodilators
 Side effects within therapeutic range
 Many drug interactions
 Smoking can affect the metabolism of
theophylline
Inhaled Corticosteroids
 Inhaled steroids now limited to moderate

symptomatic disease with 2 exacerbations per
year to reduce admission rates1
 Emerging evidence of enhanced effect of

xanthines when combined with corticosteroid
1 NICE (2004)
Mycolytics
Carbocisteine
 Reduces sputum viscosity to aid expectoration

 Reduces exacerbations of COPD in those with chronic productive
cough
 (caution in peptic ulceration / can cause gastrointestinal irritation)
Erdotin - Short course during acute exacerbation
GOLD guidelines (2007) suggest there is not enough evidence to support there use. However, there
are a group of patients in which it works well in
COPD Therapy - New Horizons
 Newer anti-inflammatory agents
 Matrix metalloproteinase inhibitors
 Specific phosphodiesterase (PDE4) inhibitors
 Cilomilast
 Rofumilast
 Piklanilast
 Anabolic steroids
 Repair agents
 Retinoic acid
 Long-acting anti-muscarinic agents
 tiotropium
Lung Reduction In Emphysema






 

 

Remove hyperinflated areas of lung:

Improve V/Q matching
Reduce resting length of respiratory muscles
Reduce Dynamic Hyperinflation
Chronic Non-Invasive Ventilation
 Domiciliary NIV for a highly

selected group of COPD
patients with recurrent
admissions requiring assisted
ventilation is effective at
reducing admissions and
minimizes costs from the
perspective of the acute
hospital 1
 1 Tuggey JM, Plant PK, Elliott MW. Thorax. 2003

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COPD

Chronic Obstructive Pulmonary

The disease is predominantly caused by smoking.

 Signiﬁcant airflow obstruction may be

 May also be related to occupational

1 Pauwels et al, 2001

The cells are fully ciliated

The cilia beat in a co-ordinated

Scanning electron micrograph showing a sheet of

 This slide shows the result of

 The damage to the cilia means

Scanning electron micrograph showing cilial and

Normal Lung Emphysema

 Dyspnoea is the reason most

1. BTS, 1997; 3. GOLD, 2003

 Smoking Cessation  MDI Therapy

 Use short acting bronchodilator PRN (beta2-

 Offer pulmonary rehab to all patients who consider themselves functionally

 Consider referral for surgery.

1 NICE Guidelines 2004

 Short Burst Oxygen

 Should be worn for 15 hrs or more a day to gain these

 Further research is required

 Improved exercise tolerance

Pharmacotherapy does not modify long-term decline, but is used to

 Signiﬁcant improvement in lung function 1-3

 better sustained improvement in lung function over 12 hours than

 Improve shortness of breath day and night 1,3

 Reduce risk of exacerbations vs. placebo 1

 Clinically signiﬁcant improvements in quality of life 4,5

 Inhaled steroids now limited to moderate

 Emerging evidence of enhanced effect of

 Reduces sputum viscosity to aid expectoration

Erdotin - Short course during acute exacerbation

Remove hyperinflated areas of lung:

 Domiciliary NIV for a highly

 1 Tuggey JM, Plant PK, Elliott MW. Thorax. 2003

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