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CHRONIC OBSTRUCTIVE
PULMONARY DISEASE ( COPD )
Epidemiology
Pathology, Pathogenesis
Prevention
Management
COPD- An Overview
Diagnosis
Systemic disease?
Chronic Obstructive Pulmonary Disease (COPD) is a
preventable and treatable disease with some significant
extra pulmonary 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.
Definition
COPD -A Neglected Disease
COPD does not kill as suddenly & unexpectedly as a myocardial infarction
More frequent in the lower socioeconomic class
Self inflicted disease-Smoker’s own fault
Limited success with primary & secondary prevention
Not so rewarding therapy
Clinically relevant only at the end of productive life
Burden of COPD- Global
COPD - 6th as cause of death in 1990
3rd as cause of death in 2020
Ischemic heart
disease (6.3
Million)
Cerebrovascular Accidents
(4.4 Million)
Lung Cancer
(0.9 Million)
Road traffic
Accidents (1.0
Million)
Measles
(1. 1 Million)
Tuberculosis
(2.0 Million)
Lower Respiratory
infection (4.3 Million)
Chronic obstructive
pulmonary Disease
(2.2 Million)
Perinatal Disease
(2.4 million)
Diarrheal Disease
( 2.9 Million)
22.9%
22.9% 22.9%
22.9%
3.3%
3.6%
4 % 7.3 %
8.7 %
8 %
Burden & Prevalence of COPD are
projected to increase
in the coming decades
Continued exposure to risk factors Changing age structure
Burden of COPD….contd
+
Risk Factors for COPD : Environmental factors
Wood fire : Biomass fuels
Environmental
Factors
Industrial pollution sulfur di
oxide particulars < 10 um
Cigarette, pipe, cigar smoking,
tobacco and cannabis
Car exhaust pollution
Mining : coal, silica &
gold cadmium fumes.
Influenza virus :
adenovirus and HIV
Bacterial infection :
streptococcus or heemophilus
Risk Factors for COPD : Host Factors
Airway hyperresponsiveness (AHR)
‘Dutch hypothesis’
Genetic factors :
(X1-antitrypsin deficiency
Host factors
Atopy :
Mast cell coated with IgE and allergen
(house dust mite)
Gender controversial
Premature baby
Small for dates
Low birth weight
Impaired lung
growth
Diet deficient in
Antioxidant vitamins (A, C & E)
Fist oil & protein
Obstructive bronchiolitis
Emphysema
Pathology of COPD
Chronic Bronchitis
Pulmonary Vascular Disease
Systemic effects
Emphysema Pulmonary Vascular Disease
Pathology of COPD ….. contd
Lung
inflammations
Anti-Oxidants
Oxidative stress
COPD
Pathology
Protoinases
Anti-proteinases
Host factors &
Amplifying mechanisms
Repair
mechanism
Pathogenesis of COPD
CD8
+lymphocyte Alveolar macrophage
Proteases
Mucus
hyper secretion Fibrosis}} Proteolysis}
Epilethial cells
Fibro blast
Connective tissue proliferation
and fibrosis
Chronic
bronchitis
Obstructive
Bronchitis Emphysema
Inflammatory Mechanism in COPD
Oxidant – Antioxidant Imbalance in COPD
Reactive oxygen
species
O2
., H2O2, OH
.
ONOO- Antioxidants
Glutathione SOD,
catalase Uric acid,
Bilirubin, Dietary :
vitamins A,C
flavonoids
Is COPD A Systemic Disease?
Systemic effect of Chronic Obstructive
Pulmonary Disease (COPD)
Muscle weakness,
wasting,osteoporosis
Cardiovascular
Endocrine
Others
Muscles, Bones
Risk of atherosclerosis
In deaths related to cardiac events
CRP levels
IGF in hypoxemic COPD
Total testosterone
Insulin resistance
Anxiety
Depression
Diagnosing COPD
Early Accurate
Why Early Diagnosis?
•Mostly irreversible disease if diagnosed late
•Significant morbidity
•Not so rewarding treatment
Early diagnosis-Effective intervention
for smoking cessation
•Lung function reversible if diagnosed early
Why Accurate?
Because most of the commonly used modalities
in diagnosing COPD do not help much in accurate
diagnosis of COPD
Medical History
 Exposure to risk factors – Smoking, others
 Symptoms pattern.
 Frequent “winter colds”.
 Co-morbidities – CAD, Malignancy, Osteoporosis.
 Impact of disease on patient’s life
 Social & family support.
Possibilities for reducing risk factors, esp smoking
cessation.
Diagnosing COPD
Chronic Cough
Dyspnea
Progressive(worsens over time)
Usually worse with exercise
Persistent (present every day)
Intermittent, unproductive.
Chronic sputum
production
Any pattern of chronic sputum
Production may indicate COPD
H/O exposure
to risk factors
Tobacco smoke
Occupational dusts and chemicals
Smoke from home cooking and
Heating fuels
Consider COPD if any of these is present
in a patient > 40 yrs of Age.
Additional Symptoms
Weight loss and
anorexia
S/O advanced COPD
(R/O TB, Br CA)
Chest tightness/
Wheezing
Non specific. More
common in severe & very
severe COPD
Ankle edema Cor Pulmonale
Depression
Physical Examination
Rarely diagnostic- low sensitivity & specificity.
•Absence of physical signs till development of
significant disease.
•Resp rate – increased, shallow breaths.
•Use of accessory muscles of resp.
•Pedal edema.
•Central cyanosis or bluish discoloration of mucosa.
•Rhonchi.
•Inspiratory crackles.
•Signs of Pulmonary
hyperinflation- Barrel
shaped chest.
Physical Examination….contd
•Reduced intensity
of breath sound.
Confirming Airflow Limitation
Spirometry is a GOLD STANDARD
Best Standardized, most reproducible &
most objective measurement
of airflow limitation
Early Diagnosis of COPD
Normal Borderline Mild Moderate Severe
Airway obstruction
35 40 45 50 55 60
Normal Hypoxemia
Normal Hyper
inflation
Resting
dyspnea
Cough & sputum Exertional
dyspnea
Symptoms
Spirometry
ABG
Chest x-Ray
AGE
Early Diagnosis of COPD
Spirometry
“Early Diagnosis” with Spirometry
45 Yrs Male
PME
History
Clinical Exam
Chest X-Ray
Spirometry
COPD – Stage I
Smoking Index - 300
Slight morning cough
NAD
FEV1 – 2.45 L (82 %)
FEV1/FVC - < 70 %
Counselling on
smoking cessation
Patient Quit
Smoking
Early Diagnosis
Smoking
Cessation
NAD
Stage of COPD
Stage – I
FEV1/FVC < 0.70
FEV1 > 80% Chronic cough
with Sputum +
Stage – II
FEV1/FVC < 0.70
FEV1 - 50% - 80%
Symptomatic
Stage – III FEV1/FVC < 0.70
FEV1 30 - 50%
↑↑ Symptomatic
Stage – IV FEV1/FVC < 0.70
FEV1 < 30%
Chronic respiratory failure +
Mild COPD
Moderate COPD
Severe COPD
Very Severe COPD
Other Investigations
Chest x-ray
• Seldom diagnostic
• Presence of bulla diagnostic
• Signs of hyperinflation
• Cor pulmonale
Diagnosis
 ABG
 Alpha-1 Antitrypsin Def Screening
 Young age < 45 yrs.
 Strong family history.
 Sperm level < 15-20%.
 Bronchodilator reversibility testing.
Diagnosis
HRCT / Spiral CT
Indications
• Diagnosis of emphysema in asymptomatic COPD
• Bronchogenic CA
• PTE / Bronchiectases
• Before lung volume reduction surgery
Echocardiography
• Cor pulmonale
Diagnosis
Exercise Testing
• 6 min walk distance
• For determining effort tolerance
Sleep studies
BMI monitoring
Diagnosis
Differential Diagnosis of COPD
S/
No.
Disease Onset of Disease Symptoms of disease
01. COPD Onset in Mild – life
Symptoms slowly
progressive.
Commonly long
smoking history rarely
ά1- antitrypsin
deficiency rarely
primary ciliary
dyskinesia.
Dyspnea during
exercise largely
irreversible airflow
limitation.
02. Asthma Onset early in life
(often childhood).
Symptoms vary from
day to day. Symptoms
at night/ early
morning.
Allergy, rhinitis, or
eczema also present
family history of
Asthma. Respond to
β2-agonists: reversible
airflow limitation.
Smoking Most important risk factor
Smoking cessation
Most beneficial
management
step for COPD
Only intervention
that reduces
accelerated
decline in lung
function
Primary Prevention
Fletcher C, Peto R: BMJ 1977
Annual Decline in Lung Function
100
75
50
25
0
25 50 75
Age ( Years)
Stopped smoking
aged 60 yr
Stopped smoking
aged 50 yr
Susceptible
smoker
(10-20%)
Death
Disability
Non smoker
Non-susceptible
smoker
Smoking Cessation
ASK Systematically identify all tobacco users at every visit.
ADVICE
ASSESS Determine willingness to make a quit attempt.
Strongly urge all tobacco users to quit.
ASSIST Aid the patient with a quit plan.
ARRANGE Schedule follow-up contact
J Am Med Assoc 2000;283:3244-54
Even a brief (3 min) period of counselling to
urge a smoker to quit results in smoking
cessation rates of 5 – 10 %
Wilson DH, etal . “Sick of Smoking’’: evaluation of a
targeted minimal smoking cessation intervention in general
practice. Med J Aug 1990 ; 152 (10) : 518 – 21
SMOKING CESSATION
Transdermal skin patches
Nasal spray
Micro tablets for sublingual use
Inhalator with a cartridge containing nicotine Chewing gum
Nicotine replacement products
Regular drug therapy
Ensure Correct inhalation
technique
Drug Therapy
Bronchodilator in Stable COPD
 Bronchodilator medications are central to symptom
management in COPD.
 The choice between β2- agonists, anticholinergic,
theophylline, or combination therapy depends on availability
and individual response in terms of symptom relief and side
effects.
 Combining bronchodilators may improve efficacy and
decrease the risk of side effects compared to increasing the
dose of a single bronchodilator.
 Bronchodilators are prescribed on an as-needed or on
a regular basis to prevent or reduce symptoms.
 Long – acting inhaled bronchodilators are more effective
and convenient.
The aerosol route is the safest, fastest and
most effective way to administer drugs in
patients suffering with asthma and COPD
and should be the method of choice in all
patients.
(GINA guidelines, GOLD guidelines)
• Jet, Ultrasonic and small volume nebulisers
• Pressurized metered dose inhalers
(pMDIs), with or without spacers (static and
non static)
• Dry powder inhalers (DPIs)
- Unit dose and Multidose
- Multi dose
AEROSOL GENERATION DEVICES
ADVANTAGES:
• Easy to use if technique proper
• Convenient – multiple doses in a
small canister
• Cheap – relatively cheaper to
manufacture
DISADVANTAGES:
• Co-ordination problems
• Cold Freon effect
• Increased oropharyngeal deposition
• CFC propellant – harms environment
Pressurized METERED DOSE INHALER
• No co-ordination required
• No cold - freon effect
• Reduced oropharyngeal deposition
• Increased drug deposition in the lungs
• As an alternative to nebulisers
SPACER
ADVANTAGES:
• Breath actuated – no co-ordination
skills required
• Easy and convenient to use
• No propellant – environmentally
friendly
DRY POWDER INHALERS
DISADVANTAGES:
• Requires a good inspiratory effort
• Carries a single dose at a time
• Capsule and drug life reduced by
moisture and humidity
• Reservoir multi-dose DPIs: Pure drug
Cohesion and static forces can reduce
dose uniformity
DRY POWDER INHALERS
• ASK THE PATIENT
• Assess the inhaler technique
• Prime importance to correct inhaler
technique
• Age
• Level of comprehension and cooperation
• Dosage of Inhaled steroids
• Acute severe attack
Which is the Best Inhaler
Device?
Therapy at each stage of COPD.
FVC1/FVC < 0.70
FEV1 > 80% predicted.
FEV1/FVC < 0.70
50% < FEV1< 80% predicted.
FEV1/FVC < 0.70
30% < FEV1< 50%
predicted.
FEV1/FVC < 0.70
FEV1< 30%
predicted or FEV1 < 50%
predicted plus chronic
respiratory failure..
Active reduction of risk factors (s); influenza vaccination
Add short- acting bronchodilator (when needed)
Add regular treatment with one or more long- acting
bronchodilators (when needed); add rehabilitation.
Add inhaled Glucocorticosteriods
if repeated exacerbations.
Add LTOT.
Consider surgical
treatments.
I: Mild II: Moderate III: Severe IV: Very Severe
Don’t forget Flu Shot
High flow systems
Complete inspiratory
demand of patient
Low flow systems
Room air used to
provide part of
inspired atmosphere
OXYGEN DELIVERY SYSTEMS
Nasal cannula
Flow rate 1-6L/min
FiO2 24-44%
Simple masks
Flow rate 6-8L/min
FiO2 40-60%
DEVICES IN LOW FLOW
SYSTEM
Continuous Oxygen
Resting PaO2 < 55 mm Hg
Hematocrit > 56%
Dependent edema
P pulmonale
Resting PaO2 of 55-59 mm Hg
LONG TERM OXYGEN THERAPY
ADV
Moderate cost
Wide availability
Fair portability
Little maint.
ADV
Low cost
Good availability
Ease of use
GAS O2 CONCENTRATOR LIQUID
ADV
Light wt
Excellent
portability
Ease of refilling
DISADV
Heavy wt
Refilling difficulty
Frequent refills
required
DISADV
Heavy wt
Poor portability
Reg maint. req
DISADV
High cost
Incompatibility
of parts
Mod maint
MODES OF OXYGEN DELIVERY
PULMONARY
REHABILITATION
‘Pulmonary rehabilitation is a multidisciplinary program of care for
patients with chronic respiratory impairment that is individually
tailored and designed to optimize physical and social performance and
autonomy.’
The principal goals of pulmonary rehabilitation are to:
(1) Reduce symptoms, disability and handicap;
(2) Improve health – related quality of life;
(3) Improve functional independence, with maximal ability to perform a
range of everyday activities;
(4) Increase physical, social and emotional well-being in every day
activities.
Why Pulmonary Rehabilitation?
Holistic approach by multidisciplinary team:
Sleep studies for selected patients
Pulmonary Rehabilitation
Exercise and physical training
Nutritional advice
Psychological assessment: Depression
Disease Education
Social & behavioral intervention
Nutrition in COPD
Nutritional assessment
• Body weight & recent weight loss
• Body mass index (BMI)
• Skin fold thickness
• Fat free mass (FFM)
Body Mass index (BMI)
< 25 kg/m2 in COPD patients associated
with increased mortality.
< 21 kg/m2 in normal Caucasians is
underweight at < 90% ideal body weight.
Dietary Assessment
• Calorie intake.
• Vitamin intake.
• Protein intake.
Treatment Options
• Improved diet and exercise.
• Antioxidants vitamin supplement.
• High calorie liquid supplement.
• Anabolic steroid.
• Recombinant human growth hormone (rhGH).
Long Term Domiciliary Oxygen Therapy (LTOT)
Improves survival, reduces secondary polycythemia & prevents
progression of pulmonary hypertension
Crokett A J, et al. (Cochrane Review). Cochrane Library Issue, issue4, 2000.
Take Home Messages
Follow five A’S in Smoking cessation
Diagnose early by Spirometry
Regular drug therapy
Pulmonary Rehabilitation
Familiarisation with GOLD International Guidelines
Good quality of life in
COPD can be a Reality
COPD.pptx

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COPD.pptx

  • 3. Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease with some significant extra pulmonary 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. Definition
  • 4. COPD -A Neglected Disease COPD does not kill as suddenly & unexpectedly as a myocardial infarction More frequent in the lower socioeconomic class Self inflicted disease-Smoker’s own fault Limited success with primary & secondary prevention Not so rewarding therapy Clinically relevant only at the end of productive life
  • 5. Burden of COPD- Global COPD - 6th as cause of death in 1990 3rd as cause of death in 2020 Ischemic heart disease (6.3 Million) Cerebrovascular Accidents (4.4 Million) Lung Cancer (0.9 Million) Road traffic Accidents (1.0 Million) Measles (1. 1 Million) Tuberculosis (2.0 Million) Lower Respiratory infection (4.3 Million) Chronic obstructive pulmonary Disease (2.2 Million) Perinatal Disease (2.4 million) Diarrheal Disease ( 2.9 Million) 22.9% 22.9% 22.9% 22.9% 3.3% 3.6% 4 % 7.3 % 8.7 % 8 %
  • 6. Burden & Prevalence of COPD are projected to increase in the coming decades Continued exposure to risk factors Changing age structure Burden of COPD….contd +
  • 7. Risk Factors for COPD : Environmental factors Wood fire : Biomass fuels Environmental Factors Industrial pollution sulfur di oxide particulars < 10 um Cigarette, pipe, cigar smoking, tobacco and cannabis Car exhaust pollution Mining : coal, silica & gold cadmium fumes. Influenza virus : adenovirus and HIV Bacterial infection : streptococcus or heemophilus
  • 8. Risk Factors for COPD : Host Factors Airway hyperresponsiveness (AHR) ‘Dutch hypothesis’ Genetic factors : (X1-antitrypsin deficiency Host factors Atopy : Mast cell coated with IgE and allergen (house dust mite) Gender controversial Premature baby Small for dates Low birth weight Impaired lung growth Diet deficient in Antioxidant vitamins (A, C & E) Fist oil & protein
  • 9. Obstructive bronchiolitis Emphysema Pathology of COPD Chronic Bronchitis Pulmonary Vascular Disease Systemic effects
  • 10. Emphysema Pulmonary Vascular Disease Pathology of COPD ….. contd
  • 12. CD8 +lymphocyte Alveolar macrophage Proteases Mucus hyper secretion Fibrosis}} Proteolysis} Epilethial cells Fibro blast Connective tissue proliferation and fibrosis Chronic bronchitis Obstructive Bronchitis Emphysema Inflammatory Mechanism in COPD
  • 13. Oxidant – Antioxidant Imbalance in COPD Reactive oxygen species O2 ., H2O2, OH . ONOO- Antioxidants Glutathione SOD, catalase Uric acid, Bilirubin, Dietary : vitamins A,C flavonoids
  • 14. Is COPD A Systemic Disease?
  • 15. Systemic effect of Chronic Obstructive Pulmonary Disease (COPD) Muscle weakness, wasting,osteoporosis Cardiovascular Endocrine Others Muscles, Bones Risk of atherosclerosis In deaths related to cardiac events CRP levels IGF in hypoxemic COPD Total testosterone Insulin resistance Anxiety Depression
  • 17. Why Early Diagnosis? •Mostly irreversible disease if diagnosed late •Significant morbidity •Not so rewarding treatment Early diagnosis-Effective intervention for smoking cessation •Lung function reversible if diagnosed early
  • 18. Why Accurate? Because most of the commonly used modalities in diagnosing COPD do not help much in accurate diagnosis of COPD
  • 19. Medical History  Exposure to risk factors – Smoking, others  Symptoms pattern.  Frequent “winter colds”.  Co-morbidities – CAD, Malignancy, Osteoporosis.  Impact of disease on patient’s life  Social & family support. Possibilities for reducing risk factors, esp smoking cessation. Diagnosing COPD
  • 20. Chronic Cough Dyspnea Progressive(worsens over time) Usually worse with exercise Persistent (present every day) Intermittent, unproductive. Chronic sputum production Any pattern of chronic sputum Production may indicate COPD H/O exposure to risk factors Tobacco smoke Occupational dusts and chemicals Smoke from home cooking and Heating fuels Consider COPD if any of these is present in a patient > 40 yrs of Age.
  • 21. Additional Symptoms Weight loss and anorexia S/O advanced COPD (R/O TB, Br CA) Chest tightness/ Wheezing Non specific. More common in severe & very severe COPD Ankle edema Cor Pulmonale Depression
  • 22. Physical Examination Rarely diagnostic- low sensitivity & specificity. •Absence of physical signs till development of significant disease. •Resp rate – increased, shallow breaths. •Use of accessory muscles of resp. •Pedal edema. •Central cyanosis or bluish discoloration of mucosa.
  • 23. •Rhonchi. •Inspiratory crackles. •Signs of Pulmonary hyperinflation- Barrel shaped chest. Physical Examination….contd •Reduced intensity of breath sound.
  • 24. Confirming Airflow Limitation Spirometry is a GOLD STANDARD Best Standardized, most reproducible & most objective measurement of airflow limitation Early Diagnosis of COPD
  • 25. Normal Borderline Mild Moderate Severe Airway obstruction 35 40 45 50 55 60 Normal Hypoxemia Normal Hyper inflation Resting dyspnea Cough & sputum Exertional dyspnea Symptoms Spirometry ABG Chest x-Ray AGE Early Diagnosis of COPD
  • 27. “Early Diagnosis” with Spirometry 45 Yrs Male PME History Clinical Exam Chest X-Ray Spirometry COPD – Stage I Smoking Index - 300 Slight morning cough NAD FEV1 – 2.45 L (82 %) FEV1/FVC - < 70 % Counselling on smoking cessation Patient Quit Smoking Early Diagnosis Smoking Cessation NAD
  • 28. Stage of COPD Stage – I FEV1/FVC < 0.70 FEV1 > 80% Chronic cough with Sputum + Stage – II FEV1/FVC < 0.70 FEV1 - 50% - 80% Symptomatic Stage – III FEV1/FVC < 0.70 FEV1 30 - 50% ↑↑ Symptomatic Stage – IV FEV1/FVC < 0.70 FEV1 < 30% Chronic respiratory failure + Mild COPD Moderate COPD Severe COPD Very Severe COPD
  • 29. Other Investigations Chest x-ray • Seldom diagnostic • Presence of bulla diagnostic • Signs of hyperinflation • Cor pulmonale Diagnosis
  • 30.  ABG  Alpha-1 Antitrypsin Def Screening  Young age < 45 yrs.  Strong family history.  Sperm level < 15-20%.  Bronchodilator reversibility testing. Diagnosis
  • 31. HRCT / Spiral CT Indications • Diagnosis of emphysema in asymptomatic COPD • Bronchogenic CA • PTE / Bronchiectases • Before lung volume reduction surgery Echocardiography • Cor pulmonale Diagnosis
  • 32. Exercise Testing • 6 min walk distance • For determining effort tolerance Sleep studies BMI monitoring Diagnosis
  • 33. Differential Diagnosis of COPD S/ No. Disease Onset of Disease Symptoms of disease 01. COPD Onset in Mild – life Symptoms slowly progressive. Commonly long smoking history rarely ά1- antitrypsin deficiency rarely primary ciliary dyskinesia. Dyspnea during exercise largely irreversible airflow limitation. 02. Asthma Onset early in life (often childhood). Symptoms vary from day to day. Symptoms at night/ early morning. Allergy, rhinitis, or eczema also present family history of Asthma. Respond to β2-agonists: reversible airflow limitation.
  • 34. Smoking Most important risk factor Smoking cessation Most beneficial management step for COPD Only intervention that reduces accelerated decline in lung function Primary Prevention
  • 35. Fletcher C, Peto R: BMJ 1977 Annual Decline in Lung Function 100 75 50 25 0 25 50 75 Age ( Years) Stopped smoking aged 60 yr Stopped smoking aged 50 yr Susceptible smoker (10-20%) Death Disability Non smoker Non-susceptible smoker
  • 36. Smoking Cessation ASK Systematically identify all tobacco users at every visit. ADVICE ASSESS Determine willingness to make a quit attempt. Strongly urge all tobacco users to quit. ASSIST Aid the patient with a quit plan. ARRANGE Schedule follow-up contact J Am Med Assoc 2000;283:3244-54
  • 37. Even a brief (3 min) period of counselling to urge a smoker to quit results in smoking cessation rates of 5 – 10 % Wilson DH, etal . “Sick of Smoking’’: evaluation of a targeted minimal smoking cessation intervention in general practice. Med J Aug 1990 ; 152 (10) : 518 – 21 SMOKING CESSATION
  • 38. Transdermal skin patches Nasal spray Micro tablets for sublingual use Inhalator with a cartridge containing nicotine Chewing gum Nicotine replacement products
  • 39. Regular drug therapy Ensure Correct inhalation technique Drug Therapy
  • 40. Bronchodilator in Stable COPD  Bronchodilator medications are central to symptom management in COPD.  The choice between β2- agonists, anticholinergic, theophylline, or combination therapy depends on availability and individual response in terms of symptom relief and side effects.  Combining bronchodilators may improve efficacy and decrease the risk of side effects compared to increasing the dose of a single bronchodilator.  Bronchodilators are prescribed on an as-needed or on a regular basis to prevent or reduce symptoms.  Long – acting inhaled bronchodilators are more effective and convenient.
  • 41. The aerosol route is the safest, fastest and most effective way to administer drugs in patients suffering with asthma and COPD and should be the method of choice in all patients. (GINA guidelines, GOLD guidelines)
  • 42. • Jet, Ultrasonic and small volume nebulisers • Pressurized metered dose inhalers (pMDIs), with or without spacers (static and non static) • Dry powder inhalers (DPIs) - Unit dose and Multidose - Multi dose AEROSOL GENERATION DEVICES
  • 43. ADVANTAGES: • Easy to use if technique proper • Convenient – multiple doses in a small canister • Cheap – relatively cheaper to manufacture DISADVANTAGES: • Co-ordination problems • Cold Freon effect • Increased oropharyngeal deposition • CFC propellant – harms environment Pressurized METERED DOSE INHALER
  • 44. • No co-ordination required • No cold - freon effect • Reduced oropharyngeal deposition • Increased drug deposition in the lungs • As an alternative to nebulisers SPACER
  • 45. ADVANTAGES: • Breath actuated – no co-ordination skills required • Easy and convenient to use • No propellant – environmentally friendly DRY POWDER INHALERS
  • 46. DISADVANTAGES: • Requires a good inspiratory effort • Carries a single dose at a time • Capsule and drug life reduced by moisture and humidity • Reservoir multi-dose DPIs: Pure drug Cohesion and static forces can reduce dose uniformity DRY POWDER INHALERS
  • 47. • ASK THE PATIENT • Assess the inhaler technique • Prime importance to correct inhaler technique • Age • Level of comprehension and cooperation • Dosage of Inhaled steroids • Acute severe attack Which is the Best Inhaler Device?
  • 48. Therapy at each stage of COPD. FVC1/FVC < 0.70 FEV1 > 80% predicted. FEV1/FVC < 0.70 50% < FEV1< 80% predicted. FEV1/FVC < 0.70 30% < FEV1< 50% predicted. FEV1/FVC < 0.70 FEV1< 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure.. Active reduction of risk factors (s); influenza vaccination Add short- acting bronchodilator (when needed) Add regular treatment with one or more long- acting bronchodilators (when needed); add rehabilitation. Add inhaled Glucocorticosteriods if repeated exacerbations. Add LTOT. Consider surgical treatments. I: Mild II: Moderate III: Severe IV: Very Severe
  • 50. High flow systems Complete inspiratory demand of patient Low flow systems Room air used to provide part of inspired atmosphere OXYGEN DELIVERY SYSTEMS
  • 51. Nasal cannula Flow rate 1-6L/min FiO2 24-44% Simple masks Flow rate 6-8L/min FiO2 40-60% DEVICES IN LOW FLOW SYSTEM
  • 52. Continuous Oxygen Resting PaO2 < 55 mm Hg Hematocrit > 56% Dependent edema P pulmonale Resting PaO2 of 55-59 mm Hg LONG TERM OXYGEN THERAPY
  • 53. ADV Moderate cost Wide availability Fair portability Little maint. ADV Low cost Good availability Ease of use GAS O2 CONCENTRATOR LIQUID ADV Light wt Excellent portability Ease of refilling DISADV Heavy wt Refilling difficulty Frequent refills required DISADV Heavy wt Poor portability Reg maint. req DISADV High cost Incompatibility of parts Mod maint MODES OF OXYGEN DELIVERY
  • 54. PULMONARY REHABILITATION ‘Pulmonary rehabilitation is a multidisciplinary program of care for patients with chronic respiratory impairment that is individually tailored and designed to optimize physical and social performance and autonomy.’ The principal goals of pulmonary rehabilitation are to: (1) Reduce symptoms, disability and handicap; (2) Improve health – related quality of life; (3) Improve functional independence, with maximal ability to perform a range of everyday activities; (4) Increase physical, social and emotional well-being in every day activities.
  • 56. Holistic approach by multidisciplinary team: Sleep studies for selected patients Pulmonary Rehabilitation Exercise and physical training Nutritional advice Psychological assessment: Depression Disease Education Social & behavioral intervention
  • 57. Nutrition in COPD Nutritional assessment • Body weight & recent weight loss • Body mass index (BMI) • Skin fold thickness • Fat free mass (FFM) Body Mass index (BMI) < 25 kg/m2 in COPD patients associated with increased mortality. < 21 kg/m2 in normal Caucasians is underweight at < 90% ideal body weight. Dietary Assessment • Calorie intake. • Vitamin intake. • Protein intake. Treatment Options • Improved diet and exercise. • Antioxidants vitamin supplement. • High calorie liquid supplement. • Anabolic steroid. • Recombinant human growth hormone (rhGH).
  • 58.
  • 59. Long Term Domiciliary Oxygen Therapy (LTOT) Improves survival, reduces secondary polycythemia & prevents progression of pulmonary hypertension Crokett A J, et al. (Cochrane Review). Cochrane Library Issue, issue4, 2000.
  • 60. Take Home Messages Follow five A’S in Smoking cessation Diagnose early by Spirometry Regular drug therapy Pulmonary Rehabilitation Familiarisation with GOLD International Guidelines
  • 61. Good quality of life in COPD can be a Reality