C O P D By Dr Sarma
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Dr.Sarma@works1
CHRONIC OBSTRUCTIVEPULMONARY DISEASE
CHRONIC OBSTRUCTIVEPULMONARY DISEASE
Dr.Sarma RVSN, M.D., M.Sc (Canada)
Consultant in Medicine and Chest,
President IMA – Tiruvallur Branch
JN Road, Jayanagar, Tiruvallur, TN
+91 98940 60593, (4116) 260593
Dr.Sarma RVSN, M.D., M.Sc (Canada)
Consultant in Medicine and Chest,
President IMA – Tiruvallur Branch
JN Road, Jayanagar, Tiruvallur, TN
+91 98940 60593, (4116) 260593
Dr.Sarma@works2
GOLDGOLDGLOBAL INITIATIVE
FOR
CHRONIC
OBSTRUCTIVE
LUNG
DISEASENHLBI AND WHO COLLABORATIVE INITIATIVENHLBI AND WHO COLLABORATIVE INITIATIVE
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WORLD COPD DAYNovember 19, EVERY YEAR
WORLD COPD DAYNovember 19, EVERY YEAR
Raising COPD Awareness WorldwideRaising COPD Awareness Worldwide
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PURPOSE OF THIS TALKRELEVANCE
Present the
Global strategy
for the Diagnosis,
Management and
Prevention of COPD
(updated Nov 2004)
BASED ON THE GOLD, NICE NAEPP, CDC, BTS,
GUIDELINES
BASED ON THE GOLD, NICE NAEPP, CDC, BTS,
GUIDELINES
1. COPD is very common
2. COPD is often covert
3. COPD is treatable
4. Culprit is smoking
5. Symptoms + DD Use spirometry
6. GP must know to Dx. Tests, Rx. and refer
7. New advances in Rx.
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DEFINITIONSDEFINITIONS
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DEFINITION OF COPDCONTENTS
1. It is chronic
2. It is progressive
3. Mostly fixed airway obstruction
4. Non reversible by bronchodilators
5. Exposure to noxious agent is a must
6. Chronic obstructive lung disease (COLD)
7. Chronic obstru. airways disease (COAD)
8. Two entities in COPD – namely
1. Chronic Bronchitis 2. Emphysema
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Antismoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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1. CHRONIC BRONCHITIS2. EMPHYSEMA
1. Productive cough
2. For a period of 3 months
3. In each of 2 consecutive years
4. Absence of any other identifiable cause of excessive sputum production
5. Airflow limitation that is not fully reversible
6. Abnormal inflammatory response to noxious agent - like smoking
1. Alveolar wall destruction
2. Irreversible enlargement of the air spaces
3. Distal to the terminal bronchioles
4. Without evidence of fibrosis
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DEFINITION OF COPDCONTENTS
ROAD – Recurrent Obstructive Airways Disease• Bronchial Asthma• Seasonal, Recurrent• Sensitizing Agent, Other Atopic disorders• Reversible obstruction, Inflammation
COLD – Irreversible, Chronic, Noxious agent• Chronic Bronchitis• Emphysema• Combination of both
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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OBSTRUCTIVE LUNG DISEASES
ASTHMA COPD
REVERSIBILITY OF AIR WAY OBSTRUTION
FULL NONE
ASTHMA
EMPHYSEMA CHRONIC BRONCHITIS
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EPIDEMIOLGY OF COPD
EPIDEMIOLGY OF COPD
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KEY POINTSCONTENTS
• Underestimated, often covert
• It is not diagnosed until clinically overt
• By that time it is moderately advanced.
• The global burden of COPD will increase
• Toll from ↑ tobacco use in alarming
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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BURDEN OF ILLNESS
• COPD is the 4th leading cause of death (next to IHD, Cancer, CVA).
• In 2000, the WHO estimated 2.74 million COPD deaths worldwide.
• In 1990, COPD was ranked 12th among the burden of diseases
• By 2020 it is projected to rank 5th.
• Often, COPD is covert
Cause Deaths
CHD 724,269
Cancer 534,947
CVA 158,060
COPD 114,318
Accidents 94,828
Diabetes 64,574
MORTALITY
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COPD PREVALENCE 2000
Cause % Change
CHD - 59%
Cancer - 64%
CVA - 39%
COPD + 163%
Accident + 32%
All other - 7%
MORTALITY TRENDS 1965 -
2000 Established Market Economies 6.98
Formerly Socialist Economies 7.35
India 4.38
China 26.20
Other Asia and Islands 2.89
Sub-Saharan Africa 4.41
Latin America and Caribbean 3.36
Middle Eastern Crescent 2.69
World 9.34
*From Murray & Lopez, 2001
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WHAT IS WRONG ?
• Cigarette smoking is the primary cause.
• USA - 47.2 million smoke, ♂ 28%, ♀ 23%
• WHO estimates 1.1 B smokers in world.
• This increases to 1.6 billion by 2025.
• Many countries, rates are ↑ alarmingly.
• In India, 4,00,000 premature deaths annually to use of biomass fuels, like cow dung cakes, open fires
• Indoor air pollution, Industrial pollution are the major risk factors in our country.
Year Consultations
1980 6.1 million
1985 7.4 million
1990 10.1 million
1995 11.8 million
2000 13.9 million
2010 ↑↑↑↑
MORBIDITY
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SMOKING - THE CULPRITSMOKING - THE CULPRIT
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RISK FACTORS FOR COPD MOST IMP RISK
• Host Factors– Genes (alpha1- anti-trypsin↓)– Hyper responsiveness– Lung growth, low BW, Age
• Exposure– Tobacco smoke, – Bio mass fuel smoke, open fires– Occupational dusts and chemicals– Chronic uncontrolled asthma– Infections, overcrowding, damp– Low socioeconomic status– Low dietary vegetable and fruit intake
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WOMEN SMOKERS
PASSIVE SMOKERS
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TENDER AGE GROUPS
COLLEGE STUDENTS
INTENSE CAUSE FOR CONCERN ?
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COPD NH – EFFECT OF SMOKING
Mortality among women smokers is on the rise globally
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PATHOGENESIS AND PATOLOGY
PATHOGENESIS AND PATOLOGY
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NOXIOUS AGENT(tobacco smoke, pollutants,
occupational exposures
COPD
PATHOGENESIS CONTENTS
Genetic factors
Respiratory infection
Others
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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1. Definition -key points
2. Burden of COPD
3. Classification
4. Risk factors
5. Pathogenesis,
6. Pathophysiology,
7. Management
8. Future research
PATHOGENESIS
INFLAMMATION
Small airway diseaseAirway inflammationAirway remodeling
Parenchymal destructionLoss of alveolar attachments
Decrease of elastic recoil
AIRFLOW LIMITATION
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1. Definition -key points
2. Burden of COPD
3. Classification
4. Risk factors
5. Pathogenesis,
6. Pathophysiology,
7. Management
8. Future research
PATHOGENESIS
ASTHMAASTHMASensitizing agent
COPDCOPDNoxious agent
Asthmatic airway inflammationCD4+ T-lymphocytes
Eosinophils
COPD airway inflammationCD8+ T-lymphocytes
MacrophagesNeutrophils
Airflow limitationCompletelyreversible
Completelyirreversible
ATOPY
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SHIFT IN THE DELICATE BALANCE
PROTEASES ANTI PROTEASES
Nutrophil elastase
Cathepsisns
MMP-1, MMP- 9, MMP – 12
Granzymes
Perforins
Alpha 1 Anti-trypsin
SLP 1, Elastin, TIMPs
COPDCOPD
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PATHOLOGY CONTENTS
• Irreversible – COPD – Why ?– Fibrosis and narrowing of the airways– Loss of elastic recoil due to alveolar
destruction– Destruction of alveolar support that
maintains patency of small airways• Reversible – Bronchial Asthma
– Accumulation of inflammatory cells, mucus, and exudates in bronchi
– Smooth muscle contraction in peripheral and central airways
– Dynamic hyperinflation during exercise
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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PATHOLOGY in COPD
Normal bronchial architecture
1. Mucus gland hypertrophy
2. Smooth muscle hypertrophy
3. Goblet cell hyperplasia
4. Inflammatory infiltrate
5. Excessive mucus
6. Squamous metaplasia
COPD
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DISSECTING MICROSCOPIC APPEARENCE
Normal parenchymal architecture
Emphysematous Lung architecture
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PATHOLOGY – COPD ASTHMA
1. Neutrophilic inflammation2. Macrophages and CD8 T cells ↑3. Altered protease/antiprotiase balance4. Tissue destruction progressive5. Alpha1 AT↓- Young age emphysema6. Goblet cell size and number ↑ in CB7. Inflammatory mediators
LT B4IL 8TNF-α
1. Eosinophilic inflamm.
2. CD4, Th2 Lymphocyte
3. Mast cells
4. Tissue destruct. less
5. Mainly allergic inflam.
6. Inflam. Mediators
LT D4
IL 4
IL 5
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PULMONARY HYPERTENSION IN COPD
Normal Pulmonary Artery
1. Duplication of elastic lamina
2. Medial hypertrophy - PH
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CLINICAL FEATURESCLINICAL FEATURES
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CHRONIC BRONCHITIS EMPHYSEMA
1. Mild dyspnea2. Cough before dyspnea starts3. Copious, purulent sputum4. More frequent infections5. Repeated resp. insufficiency6. PaCO2 50-60 mmHg
7. PaO2 45-60 mmHg
8. Hematocrit 50-60%9. DLCO is not that much ↓10. Cor pulmonale common
1. Severe dyspnea2. Cough after dyspnea 3. Scant sputum4. Less frequent infections5. Terminal RF
6. PaCO2 35-40 mmHg
7. PaO2 65-75 mmHg
8. Hematocrit 35-45%9. DLCO is decreased10. Cor pulmonale rare.
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CHRONIC BRONCHITIS EMPHYSEMA
BLUE BLOTTER PINK PUFFER
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ALPHA1 ANTITRYPSIN ↓ EMPHYSEMA
Specific circumstances of Alpha 1- AT↓include.
• Emphysema in a young individual (< 35)
• Without obvious risk factors (smoking etc)
• Necrotizing panniculitis, Systemic vasculitis
• Anti-neutrophil cytoplasmic antibody (ANCA)
• Cirrhosis of liver, Hepatocellular carcinoma
• Bronchiectasis of undetermined etiology
• Otherwise unexplained liver disease, or a
• Family history of any one of these conditions
• Especially siblings of PI*ZZ individuals.
• Only 2% of COPD is alpha 1- AT ↓
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ALPHA1 ANTITRYPSIN ↓
1. MM – A1AT 100%
2. MS – A1AT 75%
3. SS – A1AT 55%
4. MZ – A1AT 55%
5. SZ – A1AT 40%
6. ZZ – A1AT 8%
A1AT LEVELS
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1. Decreased FEV1
2. Decreased FVC
3. FEV1 < 80%
4. FEV1 ÷ FVC < 70%
5. Post bronchodilator –
no change in FEV1
6. PEF is decreased
7. FET – is prolonged
8. V Max - decreased
CLINICAL SIGNS SPIROMETRY
1. Physical exam may be negative 2. Hyper-inflated chest, Barrel chest3. Wheeze or quite breathing4. Pursed lip / accessory muscles resp.5. Peripheral edema6. Cyanosis, ↑ JVP7. Cachexia8. Cough, wheeze, dyspnea, sputum
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1. No of cigarettes / day
2. No of smoker years
3. Age at starting
4. Time of 1st cigarette
5. Desire to quit
6. Barriers to quit
7. Passive smoking
8. Occupational expo.
9. Domestic pollution
MRC DYSPNOEA SCALE ABOUT SMOKING
Grade Degree of breathlessness - related activity
0 No breathlessness except on strenuous exercise
1 Short of breath when walking uphill or while hurrying to catch a bus or train
2 Walks slower than contemporaries or has to stop for breath while walking alone
3 Stops for breath on walking 100 m or after 2 or 3 minutes continuously
4 Too breathless to leave house or breathless while dressing
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1. Coal mining
2. Cotton dust
3. Cement dust
4. Oil fumes
5. Cadmium fumes
6. Grain dust –
Rice millers
Grain handlers
Flour millers
OXYGEN COST DIAGRAM OCCUPATIONAL
Slow
up
hill
wal
king
Med
ium
up
hill
wal
k
Brisk
wal
king
on
leve
l
0 10
Sleep
ing
Sittin
g
Slow
wal
king
Ligh
t sh
oppi
ngHea
vy s
hopp
ing
Med
ium
wal
king
Self w
ashi
ng
Bed m
akin
g
Brisk
up h
ill
wal
k
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1. Hypercapnic RF pts.
2. 1029 patients studied
3. 89% survived acute hospitalization for RF
4. Only 51% are alive at 2 years of follow-up
5. Prognostic factors are• Severity of RF• Low BMI• Older age
• Low PaO2/FIO2
PROGNOSTIC FACTORS ‘SUPPORT’ STUDY
Several factors affect survival in COPD. • Age • Smoking status • Pulmonary artery pressure • Resting heart rate • Airway responsiveness • Hypoxemia• Most importantly the level of FEV1
• Use of long term oxygen therapy
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1. Different etiology
2. Different prognosis
3. Different therapy
4. Different response to therapy
5. DD includes
Bronchial Asthma
Bronchiectasis- CSLD
Bronchogenic Ca.
DIFF. Dx. of COPD & ASTHMA WHY D.D WITH
ASTHMA ? Clinical COPD ASTHMA
Smoker Nearly all May or may not be
Age < 35 Rare Nearly all
Sputum Productive Mucoid or none
Dyspnea Persistent Episodic
Course Progressive Variable, static
Spirometry Obstructive Normal or Obstru.
Reversibility Change < 15% Change > 15%
Most IMP Rx. IBD (Ipa+Salm) ICS
Anti leukotrn. Not useful Useful ad on Rx.
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COPD IMAGESCOPD IMAGES
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CHEST SKIAGRAMS OF EMPHYSEMA
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V- P MISMATCH NUCLEOTIDE IMAGING
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CHEST SKIAGRAM OF CHRONIC BRONCHITIS
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CHEST LATERAL VIEW CHRONIC BRONCHITIS
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HRCT – NORMAL CHEST
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HRCT – EMPHYSEMA
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HRCT – EMPHYSEMA
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ASSESSMENT OF STABLE COPD
ASSESSMENT OF STABLE COPD
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1. Prevent disease progression
2. Relieve symptoms
3. Improve exercise tolerance
4. Improve health status
5. Prevent and treat exacerbations
6. Prevent and treat complications
7. Reduce mortality
8. Minimize side effects from treatment
MANAGEMENT OF COPD Rx. OBJECTIVES
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD Education Pharmacologic Non-pharmacologic
4. Manage exacerbations
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ASSESSMENT OF COPD MANAGEMENT
Diagnosis of COPD is based on
1. H/o exposure to noxious agent
2. Presence of Air flow limitation
3. Non-reversibility of the limitation
4. Chronic productive cough
5. Copious sputum, Dyspnea +/-
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage exacerbations
ASSESSMENT OF COPD
SYMPTOMS EXPOSURE
COUGH
SPUTUM
DYSPNEA
SMOKING
OCCUPATION
INDOOR / OUTDOOR
Air Pollution
SPIROMETRY IS A MUST
+ or -
More than one month
Age 35 +
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ASSESSMENT OF COPD MANAGEMENT
Diagnosis of COPD
• Spirometry is the Gold Standard
• Every COPD suspect must get spirometry test done
• Like ECG, Spirometry is essential
• Arterial blood gas tensions are needed if the FEV1 < 40%
• Respiratory failure, Corpulmonale
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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OTHER INVESTIGATIONS
1. Serial spirometry tests2. Pulse Oximetry3. Alpha1 Anti-trypsin levels
4. TLCO
5. HRCT6. ECG7. ECHO8. Sputum culture
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
TESTS
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NORMAL AND COPD SPIROMETRY
0
5
1
4
2
3
Lit
er
1 65432
FVC
FVC
FEV1
FEV1
Normal
COPD
3.900
5.200
2.350
4.150 80 %
60 %NormalCOPD
FVCFEV1 FVCFEV1/
Seconds
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WITH BRONCHODILATOR REVERSIBILITY PROTOCOL
1. Patient must be clinically stable
2. Patient should avoid
Short acting βagonists for 6 hours
Long acting βagonists for 12 hours
SR Theophylline for 24 hours
3. Baseline spirometry
4. Nebulize Salbuamol 2.5 mg + Ipatropium 500mg for 15 minutes with Nacl
5. Wait for 30 minutes
6. Repeat spirometry
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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WITH STEROIDS REVERSIBILITY PROTOCOL
1. Spirometry before and after steroid
2. Two weeks treatment with 30 mg Prednisolone daily or
3. Six weeks treatment with 800 mcg to 1000 mcg of inhaled betamethasone/day
4. Results to be interpreted.
Look for steroid contraindications
This predicts the COPD group who will benefit
from inhaled or systemic steroids
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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WHAT IS REVERSIBILITY ? TESTING
Criteria for reversibility of obstruction
• Spirometry is the Gold Standard
• Every COPD suspect must get spirometry test done and reversibility assessed
• Post bronchodilator FEV1 must show increase of at least 200 ml ↑
• And the increase should be at least 15% of the baseline FEV1 value
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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1. Severity of symptoms
2. Stages of COPD
3. Frequency and severity of exacerbations
4. Presence of complications of COPD
5. Presence of respiratory insufficiency
6. Co-morbidity
7. General health status
8. Number of medications needed to manage the disease
SEVERITY OF COPD FACTORS
STAGES OF COPD Stage 0 Normal spirometry but with
(At risk) chronic sym. – sputum, dyspnea Stage 1 FEV1 > 80%
Mild FEV1 ÷ FVC is < 70%
Stage 2 FEV1 < 80% but > 50%
Moderate FEV1 ÷ FVC is < 60%
Stage 3 FEV1 < 50% but > 30%
Severe FEV1 ÷ FVC is < 40%
Stage 4 FEV1 < 30%
V. severe FEV1 ÷ FVC is < 30%
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RISK REDUCTIONSTRATEGIES
RISK REDUCTIONSTRATEGIES
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1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage exacerbations
IF ONE QUITS SMOKING NO TOMORROW!
1. Treatment starts with reducing risks – pack years concept*
2. Studies have shown that with smoking cessation
• The rate of decline in lung function slows
• There will be definite clinical improvement in symptoms
* Packets per day x Years of smoking = Pack Years
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5. Withdrawal
4. Boredom
3. Sense of deprivation or depression
2. Emotional upset and stress
1. Alcohol abuse !
One devil replaced by another devil
5 RELAPSE TRIGGERS
1. ↓Exposure to smoking, noxious agn
2. Smoking cessation is the single most
effective - and cost effective -
intervention to reduce the risk of
developing COPD
3. It stops progression of COPD
RISK FACTORS REDUCTION
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1. Antidepressant - Bupropion
2. In psychological dependence on nicotine
3. Useful in individuals with or at risk for depression–
4. Contraindicated in drug interactions or seizure disorder
NICOTINE REPLACEMENTS DRUG TO QUIT ?
• Helpful for physical withdrawal symptoms• Can be dosed according to degree of use• Costs the same as daily smoking habit• Most products of NRT - cautious use in
cardiac patients• Bupropion may be alternative to NRT• Nicotex or Smoquit SR 150 b.i.d • Patch is more constant level, sprays &
inhaler a more rapid effect
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COPD MANAGEMENTLATEST GUIDELINESCOPD MANAGEMENTLATEST GUIDELINES
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MANAGEMENT
• Prevent disease progression
• Relieve symptoms
• Improve exercise tolerance
• Improve health status
• Prevent and treat complications
• Prevent and treat exacerbations
• Reduce mortality
1. Stable COPD
2. Exacerbations
3. Respiratory failure
4. Cardiac failure
GOALS OF MANAGEMENT
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HOW TO ASSESS?
1. Spirometric assessment
2. Walking distance
3. Dyspnea indices
4. Symptom scores
5. Exacerbation rates
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage exacerbations
OUTCOME MEASURES
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BRONCHO- DILATORS
• IBD are the main stay
• As when needed basis
• The main drugs are
– β2 - Agonists (Salbutamol group)
– Anticholinergics (Ipatropium group)
– Their combination
– ?? Theophylline
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage exacerbations
MANAGEMENT - IBD
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MANAGEMENT
1. IBD do not alter the pathology
2. Drug Rx. is to improve
symptoms and ↓complications.
3. But stopping smoking will halt
COPD
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage exacerbations
BUT UNFORTUNATELY
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THE RULES
1. NO systemic steroids in stable COPD2. Inhalation treatment is BEST3. Salmeterol is the FIRST choice4. Ipatropium is the SECOND choice5. Salbutamol for short bursts6. Inhaled steroids THIRD choice7. Combination Ipa + Salmet inhalers beneficial8. Oral β2 Agonists FOURTH choice
9. Theophyllins ? role – LA preps. No injectables10. Oxygen therapy for exacerbations and RF
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage exacerbations
MANAGEMENT RULES
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BRONCHO DILATORS
• Bronchodilators in COPD have been shown to be ineffective in modifying the long-term decline in lung function which is the hallmark of this disease (Class 1).
• There will be no ↑ in FEV1 or FEV1 ÷ FVC
• But, ↑ in exercise capacity demonstrated. Ipratropium and Salmeterol have been shown to improve COPD clinical status
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage exacerbations
IS IT A PARADOX ?
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SYNERGISM BRONCHODILATION
IPATROPIUM SABA and LABA
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ß AGONISTS
1. Direct action on the beta2 receptors in the bronchial smooth muscle – relaxation
2. Salbutamol most widely used3. In COPD 1 mg is the maximum dose4. Short acting – every 4 to 6 hours5. Salmeterol is long acting – 12 hours6. Slow onset, dose 50 μg b.i.d7. Formoterol still longer -12 μg b.i.d8. Side effects – tremors, tachycardia etc.,
1. Selective ß agonists
2. Short acting drugs
3. Long acting drugs
4. Oral medication
5. Inhaled form
BRONCHODILATORS
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ANTI ACH
1. ↑ Cholinergic drive is in the bronchii
2. Anti-cholinergics ↓resting bronchial tone
3. Three muscarinic receptors M1, M2, M3
4. Ipatropium, Oxitropium – onset slower than ß agonists – but more effective
5. Sustained broncho-dilatation – up to 8 h
6. Have influence on sleep quality in COPD
7. Ipatropium optimal dose 80 μg as inhaler
8. Tiotropium – selective to M1, M3 receptors
9. It is long acting – once a day – dose 40 μg
1. Anti-cholinergics
2. Short acting drugs
3. Long acting drugs
4. Inhaled forms
5. Combination with beta agonists
BRONCHODILATORS
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ORAL STEROIDS
Inhaled Glucocorticoids• In stage I and II COPD – no role to play• Betamethasone, Budisonide, Fluticasone• Inhaled steroids are preferable and they
reduce the # of episodes of exacerbation• To be used in stage III and stage IV COPD• They are useful in short bursts in acute
exacerbations• In people with significant asthma component
they are found useful• No role for long acting steroid injections
1. Asthmatic component
2. Quick recovery from acute exacerbations
3. Delays next exacerb.
4. Only small number of patients sustained improvement
5. Similar to asthmatics
6. Significant risk of side effects
CORTICOSTEROIDS
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THEOPHYLLINE
1. Assumed to relax the airway smooth muscle
2. At therapeutic concentration NO direct action on the bronchial smooth muscle
3. Toxicity – Many drug interactions
4. Low therapeutic index - Poor safety window
5. Need to monitor blood levels frequently
6. Adverse effects on liver and in elderly
7. Their use is at best questionable
8. Never injectable – in may countries banned
9. SR prep has some add on value
1. Deriphyllin group
2. Nausea, tachycardia
3. Fatal arrhythmias
4. Interactions with drugs - Macrolides
5. Smokers have higher theophylline toxicity
6. Already tachycardiac
7. Only oral - if at all
BRONCHODILATORS
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INHALED Rx.
• IBD is the preferred drugs
• LABA + Tiotropium is best
• LABA + TIO + ICS for Stage III, IV
• Combination is better than increasing individual drugs
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage exacerbations
MANAGEMENT
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NO SYSTEMIC STEROIDS
• No systemic steroids because of • unfavorable benefit-to-risk ratio • Exercise training programs, • LTOT > 15 hours per day for RF• LTOT increases survival
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage exacerbations
MANAGEMENT
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MANGEMENTAS PER STAGING
MANGEMENTAS PER STAGING
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AT RISK
• Avoidance of risk factors• Stop smoking• Influenza vaccine• Regular follow up spirometry
1. Chronic symptoms
2. Cough
3. Phlegm
4. Dyspnea
5. H/o smoking
6. Spirometry Normal
MANAGEMENT - STAGE 0
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MILD COPD
• Avoidance of risk factors• Stop smoking• Influenza vaccine• Regular follow up spirometry +• SABA + IPATROP• Inhaled route
1. Chronic symptoms
2. Cough
3. Phlegm
4. Dyspnea
5. H/o smoking
6. Spirometry abnormal
7. FEV1 > 80% but
8. FEV1 / FVC < 70%
MANAGEMENT – STAGE I
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MODERATE COPD
• Avoidance of risk factors• Stop smoking• Influenza vaccine• Regular follow up spirometry• SABA + IPA inhalations +• LABA or TIOTROP or BOTH in inhaled• Pulmonary Rehabilitation
1. Chronic symptoms
2. Cough
3. Phlegm
4. Dyspnea
5. H/o smoking
6. Spirometry abnormal
7. FEV1 < 80% but > 50%
8. FEV1 / FVC < 60%
MANAGEMENT – STAGE II
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SEVERE COPD
• Avoidance of risk factors• Stop smoking• Influenza vaccine• Regular follow up spirometry• SABA + IPA inhalations +• LABA or TIOTROP or BOTH inhaled• Pulmonary Rehabilitation• ICS – Budesonide• LTOT at least 15 hours per day
1. Chronic symptoms
2. Cough
3. Phlegm
4. Dyspnea
5. H/o smoking
6. Spirometry abnormal
7. FEV1 < 50% but > 30%
8. FEV1 / FVC < 40%
MANAGEMENT – STAGE III
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V. SEVERE COPD
• Avoidance of risk factors• Stop smoking• Influenza vaccine• Regular follow up spirometry• SABA + IPA inhalations +• LABA or TIOTROP or BOTH inhaled• Pulmonary Rehabilitation• ICS – Budesonide• LTOT at least 15 hours per day• Oral steroids in short bursts• Surgical treatments
1. Chronic symptoms
2. Cough
3. Phlegm
4. Dyspnea
5. H/o smoking
6. Spirometry abnormal
7. FEV1 < 30%
8. FEV1 / FVC < 30%
9. Chronic Resp. Failure
MANAGEMENT – STAGE IV
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DRUG DELIVERYSYSTEMS - OPTIONS
DRUG DELIVERYSYSTEMS - OPTIONS
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DRUG DELIVERY
• MDI – Metered Dose Inhalers• Rotahalers, Diskhalers• Spacehalers• Nebulizers• Oxygen mixed delivery• Oral tablets, syrups ??• Parenteral – I.M or I.V use ????
1. Dexterity
2. Hand grip strength
3. Co-ordination
4. Severity of COPD
5. Educational level
6. Age of the patient
7. Ability to inhale and synchronize
DRUG DELIVERY - OPTIONS
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NEBULISED THERAPY
1. Severe breathlessness despite using inhalers 2. Assessment should be done for improvement3. Choice between a facemask or mouth piece4. Equipment servicing and support are essential5. Dosage 0.5 ml of Ipatropium +
0.5 ml of Salbutamol + 5 ml of NaCl (not DW)6. If decided to use ICS (FEV1 < 50%) –
0.5 ml of Budusonide is added to the above6. 15 minutes and slow or moderate flow rate7. Can be repeated 2 to 3 times a day – Mouth Wash
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EDUCATION ANDREHABILITATIONEDUCATION ANDREHABILITATION
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REHABILITATION
For the lungs to get more air
PURSED-LIP BREATHING(like breathing out slowly into a straw)
INHALE EXHALE
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1. Sit comfortably and relax your shoulders.
2. Put one hand on your abdomen. Now inhale slowly through your nose. (Push your abdomen out while you breathe in)
3. Then push in your abdominal muscles and breathe out using the pursed-lip technique. (You should feel your abdomen go down)
Note: • Repeat the above maneuver three times and then take a little rest.• This exercise can be done many times a day.
REHABILITATION
For the lungs to get more air
DIAPHRAGMATIC BREATHING
Sit comfortably and 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
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HEALTH EDUCATION – TEAM WORK
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EXACERBATIONSRESP. FAILURE
EXACERBATIONSRESP. FAILURE
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OXIGENERATOR
• Diagnosis uncertain• Disproportionate symptoms• Persistent symptoms• Development of lung cancer• Pulmonary rehabilitation• Nebulizer assessment• Oxygen assessment
MANAGEMENT – REFERRAL
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WHEN SUSPECT?
1. Pulmonary embolism2. Pneumothorax – rupture of bullae3. Myocardial infarction4. Left ventricular failure5. Acute pneumonia6. Bronchogenic carcinoma
1.↑ in symptoms
2.↑ in sp purulence
3.↑ in sp volume
4.Fever, chills
5.Ankle edema
6.Cyanosis
7.↓ Consciousness
D.D. of EXACERBATIONS
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WHAT EXTRA ?
1. Exacerbations of symptoms requiring Rx. are important clinically in COPD.
2. The most common causes of exacerbation are Infection of the bronchial tree and Air pollution and ↑ in smokingIn 35% of cases cause is not known
3. Systemic corticosteroids – oral better4. Antibiotics in short bursts – what to give5. NIPPV – Non invasive intermittent
positive pressure ventilation - Home
1. Oxygen therapy
2. NIPPV mostly or
3. Macha. Ventilation
4. Ipatropium inhalation
5. SA - Beta agonists
6. No theophylline group
7. Narrow spectrum antibiotics – 2 wks
8. Oral steroids for 2 wk
9. Diuretics may help
MANAGE EXACERBATIONS
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LONG TERM OXYGEN THERAPY
• Pulse oximetry to know PaO2
• Arterial blood gas saturation monthly• Review LTOT every year• Oxygen concentrators - oxygen cylinders• Fire warning – smoking• Ambulatory oxygen therapy – O2 cylinders,
liquid oxygen• SBOT - Short burst OT – Exacerbations.• NIPPV in patients with ↓respiratory drive
INDICATIONS
1. FEV1 < 30% must
2. Consider if < 50%
3. PaO2 < 90%
4. PaCO2 > 60%
5. Cyanosis
6.↑ JVP, Pedal edema
7. Pulmonary HT
8. Polycythemia
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CORPULMONALE
• LTOT• Diuretics, Sodium restriction• ACEi • Alpha blockers• Digoxin• Heart failure management
FEATURES
1. Increasing dyspnea
2. Peripheral oedema
3.↑ venous pressure
4. Parasternal heave
5. Loud pulmonary second heart sound
6. ECG changes of RVH and PH
7. Echo evidence
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RESP. FAILURE
1. Pulmonary hypertension2. Right ventricular hypertrophy3. Right ventricular diastolic dys. function4. Right ventricular systolic dysfunction5. Corpulmonale – Right heart failure6. Acute respiratory insufficiency7. Life threatening respiratory failure8. Hypercapnia, Severe hypoxia9. Intubation and IPPV10. Managing RVF and RF – ICU care
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Management of exacerbations
RESPIRATORY FAILURE
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SURGERY
1. Increasing dyspnea2. Single large emphysematous bulla3. Severe - FEV1 < 35% but > 20%4. Upper lobe emphysema5. PaCo2 not more than 55%
6. TLCO must be at least 20%
7. Age less than 658. Severe pulmonary hypertension
1. Bullectomy
2. LVRS - Lung volume reduction surgery
3. Single lung transplant
LUNG RESECTION
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WHAT NOT !
• Pneumococcal vaccine may be given• Early initiation of O2 shown to ↑ survival• Prolonged use of inhaled steroids –
long acting better – 2 weeks duration• Alpha1 anti-trypsin (Prolastin, Aralast)• Antibiotics in short bursts for exacerbations• N-Acetyl cysteine (NAC) is shown useful• Immuno-modulators are under trial• Calcium and vitamin D supplementation
1. No Anti-tussives
2. Mucolytics ??
3. No prophylactic antibiotics
4. No long term antibiotics
5. No systemic steroids
6. No narcotics
7. No vigorous exercise
8. No with holding the benefits of Oxygen
WHAT ELSE WE CAN GIVE
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COPD - FUTURE DEVELOPMENTSCOPD - FUTURE DEVELOPMENTS
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NEXT DECADE
• Emphasis on early diagnosis• Effective anti smoking services• COPD will be primary care issue by GP• New drug development for COPD perse• Tiotropium takes a center stage• New M1 and M3 blockers are in line• PDE4 inhibitors – for bronchodilatation• Drugs to ↓Neutrophilic inflammation• Mediator antagonists - ↓inflammation
1. COPD will increase
2. Mortality will increase
3. Dx. facilities increase
4. Quit smoking a must
5. Industrial pollution ↑
6. Newer drugs
7. New drug delivery
8. Oxygen Therapy ↑
FUTURE DEVELOPMENTS
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• COPD is no more a specialists concern – it is ours !• It is alarmingly increasing – It is preventable• Please differentiate Asthma and COPD• Use spirometry, peak flow meter - just as ECG • Don’t embark on Deri + Bet iv for all breathlessness• Don’t use Theophylline as far as possible• Inhalation therapy is the best – Drug delivery choices• Don’t spare any body from early oxygen therapy• And finally, motivate smokers to quit smoking
TAKE HOME MESSAGES
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SELF SCREENINGSELF SCREENING
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Do you know what COPD is ? This chronic lung disease is a major cause of illness. Many people have it and yet don’t know it.
If you answer these questions, it will help you find out if you could have COPD.
1. Do you cough several times most days? Yes ___ No ___
2. Do you bring up phlegm or mucus most days? Yes ___ No ___
3. Do you get out of breath more easily than others your age? Yes ___ No ___
4. Are you older than 40 years? Yes ___ No ___
5. Are you a current smoker or an ex-smoker? Yes ___ No ___
If you answered yes to three or more of these questions, ask your doctor if you might have COPD and should have a simple breathing test. If COPD is found early, there are steps you can take to prevent further lung damage and make you feel better.
Take time to think about your lungs……Learn about COPD!
Do you know what COPD is ? This chronic lung disease is a major cause of illness. Many people have it and yet don’t know it.
If you answer these questions, it will help you find out if you could have COPD.
1. Do you cough several times most days? Yes ___ No ___
2. Do you bring up phlegm or mucus most days? Yes ___ No ___
3. Do you get out of breath more easily than others your age? Yes ___ No ___
4. Are you older than 40 years? Yes ___ No ___
5. Are you a current smoker or an ex-smoker? Yes ___ No ___
If you answered yes to three or more of these questions, ask your doctor if you might have COPD and should have a simple breathing test. If COPD is found early, there are steps you can take to prevent further lung damage and make you feel better.
Take time to think about your lungs……Learn about COPD!
Could it be COPD?Could it be COPD?
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ASTHMA V/s COPDTake HOME GUIDEASTHMA V/s COPDTake HOME GUIDE
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ASTHMA V/s COPDASTHMA V/s COPD
ASTHMA COPD
Sensitizing trigger needed Chronic exposure -Noxious
Innate Atopy is essential Any body may be effected
No noxious external agent Smoking is the noxious ag.
ETIOLOGICAL BASIS
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ASTHMA V/s COPDASTHMA V/s COPD
ASTHMA COPD
Primarily Allergic Inflamm. Destructive Inflammation
Secondary bronchospasm Primary ↑ in bronchial tone
Small airways - bronchioles Disease of alveloli, bronchi
No destruction or fibrosis Alveolar destruc. Br fibrosis
PATHOLOGY
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ASTHMA V/s COPDASTHMA V/s COPD
ASTHMA COPD
Recurrent allergic inflamm. Progressive destr. inflamm.
Airway remodeling occurs Emphysema, Bronchial fibr.
↑↑ IgE + other atopic disea. ↑ Proteases, ↓in antiprote.
CD4 T, Mast cells, Eosino CD 8 T, MF, Neutrophils
LT D4, IL 4, IL 5, - Th2 LT B4, IL 8, TNF-α
PATHOGENESIS
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ASTHMA V/s COPDASTHMA V/s COPD
ASTHMA COPD
Young subjects, any age Age always > 35 yrs, smoke
Episodic, recurrent, normal Chronic, progressive, Exaca
Sputum mucoid or none Sputum purulent & copious
Episodic dyspnea – moder. Progressive dyspn, Hr. Gr.
Seasonal symptoms Perennial symptoms
CLINICAL FEATURES
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ASTHMA V/s COPDASTHMA V/s COPD
ASTHMA COPD
Normal or obstructive Always obstructive pattern
FEV1 < 80% but > 60% FEV1 < 70% may be < 40%
FEV1 ÷ FVC < 70% FEV1 ÷ FVC < 60%
Reversible - > 15 % ↑ Irreversible - < 15 % ↑
Resp. failure rare Resp. failure,Corpulmonale
SPIROMETRY
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ASTHMA V/s COPD. - Rx.ASTHMA V/s COPD. - Rx.ASTHMA COPD
Relievers and Preventers Quitting of smoking crucial
ICS are the main stay LABA + Antibiotics – Ac. exa
SABA for acute attacks SABA not much, ICS useful
Ipatropium add on only Ipatrop., Tiotrop. are first line
LTA are very useful LTA have no role at all
Mast cell stabilizers useful Cromolyn, Ketotifen no use
LTOT not needed mostly LTOT must in stage III and IV
Oral steroids have little role Oral steroids in stage III & IV
SR Theophylline?? some role SR Theophylline contraindic.
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“The old order changethyielding place to new;Lest, one good custom
should corrupt the world.”
“The old order changethyielding place to new;Lest, one good custom
should corrupt the world.”
This is most pertinent today to Asthma and COPD
This is most pertinent today to Asthma and COPD
Tennyson Sir Lord, AlfredTennyson Sir Lord, Alfred
Holm and Harris & NEJM
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PREVENT COPDPREVENT COPD
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THE DEADLIEST DEVILTHE DEADLIEST DEVIL
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SURE TO GRAVESURE TO GRAVE
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AND FINALLYAND FINALLY
Tell me what harm smoking
does not cause ??
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TELL ME THE ORGAN SPARED
1. IHD, MI, ↑ Restenosis2. Atherosclerosis – PVD, IR, ↑ DM3. Oxidation of LDL, ↑ LDL, ↓ HDL, ↑ TG4. COPD, Lung Cancer5. Tremors, Peripheral neuritis6. APD, NUD, Oro-pharyngeal Cancers7. Osteoporosis8. Poor fetal development9. Nicotine dependence10. Wasteful expenditure
1. The Heart
2. Blood vessels
3. Metabolic effects
4. Lungs
5. Nervous system
6. G I tract
7. Bones
8. Fetus in utero
9. The psyche
10.The Purse
PROVEN DISASTERS
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Most of these effects have dose-response relationship.
Most of them are reversible if smoking is stopped early.
Reducing the # reduces the risk – inverse response.
If we are a smoker, let us quit smoking – set an example.
Let us motivate every month at least one person to quit.
What right we have, to make others passive smokers?
The Onus here is on usThe Onus here is on us
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Pledge to stop smokingPledge to stop smoking
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WHAT CAN WE DO ??WHAT CAN WE DO ??
120Dr.Sarma@works
If, in patients I treat, I have
• Not controlled his DM
• Not evaluated for IHD
• Not kept BP to goal
• Not controlled lipids
• Not advised the obese
• Not persuaded a smoker
• Not prevented OS
• Not health educated and
I have not updated my K
Not shared what I have
MY SINS
SINS
PUNYAS
IF CARE NOT TO DO THESE – THEN ALL
121Dr.Sarma@works
1. My possessions
2. My positions
3. My achievements
4. My abilities
5. My privileges
6. My prayers
7. My visits to temples
8. My scriptural K
9. My rituals
MY GAINS HAVE NO MEANING & ARE MERELY FUTILE
SINS
PUNYAS
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REMEMBER, WE ARE BLESSED
WITH THE OPPORTUNITY
REMEMBER, WE ARE BLESSED
WITH THE OPPORTUNITY
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Om Asatho maa sad gamaya
Om Tamaso maa jyothir gamaya
Om Mrityor maa amritam gamaya
Om Sarveshaam swasthir bhavathu
Om Sarveshaam shaantir bhavathu
Om Shaantihi Shaantihi Shaantihi ||
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A CD format of today’s presentation is ready
1. COPD, Asthma and basics of spirometry
In addition it, also contains
2. ECG workshop presented earlier
3. Guidelines on Hypertension treatment
This can be used in Computer & DVD player
Important Announcement
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1. ACCP www.chestnet.org2. ATS www.thoracic.org3. BTS www.brit-thoracic.org.uk4. COPD profess.
www.copdprofessional.com5. GOLD www.goldcopd.com6. NICE www.nice.uk.org7. Chest Net www.chestnet.net8. CDC www.cdc.nih.gov9. NAEPP www.naepp.nhlbi.org10.COPD Rapid series by ELSEVIER
Resources for COPD and Asthma
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Dr.Sarma RVSN, M.D., M.Sc (Canada)
JN Road, Jayanagar, Tiruvallur, TN
+91 98940 60593, (4116) 260593
PLEASE CONTACT US
Dr. Kumaran.M, B.Sc., M.B.B.S.,
10 North Raja St, Tiruvallur, TN
+91 98941 10450, (4116) 260288
WE WILL MEET AGAIN SOON
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NANRI,
VANAKKAM
NANRI,
VANAKKAM