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CHRONIC OBSTRUCTIVE
PULMONARY 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
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GOLDGLOBAL INITIATIVE
FOR CHRONIC
OBSTRUCTIVE
LUNG
DISEASE
NHLBI AND WHO COLLABORATIVE INITIATIVE
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WORLD COPD DAY
November 19, EVERY YEAR
Raising 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
1. COPD is verycommon
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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DEFINITIONS
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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 COPDnamely
1. Chronic Bronchitis 2. Emphysema
1. Definition - Key points2. Epidemiology
3. Risk factors
4. PathogenesisPathol
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 cough2. For a period of 3 months
3. In each of 2 consecutive years
4. Absence of any other identifiablecause of excessive sputum production
5. Airflow limitation that is not fully reversible
6. Abnormal inflammatory response to
noxious agent - like smoking
1. Alveolar walldestruction
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
ROADRecurrent Obstructive Airways Disease Bronchial Asthma
Seasonal, Recurrent
Sensitizing Agent, Other Atopic disorders
Reversible obstruction, Inflammation
COLDIrreversible, Chronic, Noxious agent
Chronic Bronchitis
Emphysema
Combination of both
1. Definition - Key points2. Epidemiology
3. Risk factors
4. PathogenesisPathol
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
EMPHYSEMACHRONIC
BRONCHITIS
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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 points2. Epidemiology
3. Risk factors
4. PathogenesisPathol
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 ofdeath (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 CULPRIT
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RISK FACTORS FOR COPDMOST 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 NHEFFECT OF SMOKING
Mortality among women smokers is on the rise globally
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PATHOGENESIS AND
PATOLOGY
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NOXIOUS AGENT(tobacco smoke, pollutants,
occupational exposures
COPD
PATHOGENESISCONTENTS
Genetic factors
Respiratoryinfection
Others
1. Definition - Key points2. Epidemiology
3. Risk factors
4. PathogenesisPathol
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. Management8. Future research
PATHOGENESIS
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1. Definition -key
points
2. Burden of COPD
3. Classification
4. Risk factors
5. Pathogenesis,
6. Pathophysiology,
7. Management8. Future research
PATHOGENESIS
ATOPY
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SHIFT IN THE DELICATE BALANCE
PROTEASES ANTI PROTEASES
Nutrophil elastase
Cathepsisns
MMP-1, MMP- 9, MMP12
GranzymesPerforins
Alpha 1Anti-trypsin
SLP 1, Elastin, TIMPs
COPD
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PATHOLOGYCONTENTS
IrreversibleCOPDWhy ? Fibrosis and narrowing of the airways
Loss of elastic recoil due to alveolardestruction
Destruction of alveolar support thatmaintains patency of small airways
ReversibleBronchial Asthma
Accumulation of inflammatory cells,mucus, and exudates in bronchi
Smooth muscle contraction in peripheraland central airways
Dynamic hyperinflation during exercise
1. Definition - Key points2. Epidemiology
3. Risk factors
4. PathogenesisPathol
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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PATHOLOGYCOPDASTHMA
1. Neutrophilic inflammation2. Macrophages and CD8 T cells
3. Altered protease/antiprotiase balance
4. Tissue destruction progressive
5. Alpha1AT- Young age emphysema6. Goblet cell size and number in CB
7. Inflammatory mediators
LT B4
IL 8TNF-
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 FEATURES
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CHRONIC BRONCHITISEMPHYSEMA
1. Mild dyspnea2. Cough before dyspnea starts
3. Copious, purulent sputum
4. More frequent infections
5. Repeated resp. insufficiency
6. PaCO250-60 mmHg
7. PaO245-60 mmHg
8. Hematocrit 50-60%
9. DLCO is not that much
10. Cor pulmonale common
1. Severe dyspnea2. Cough after dyspnea
3. Scant sputum
4. Less frequent infections
5. Terminal RF
6. PaCO2 35-40 mmHg
7. PaO265-75 mmHg
8. Hematocrit 35-45%
9. DLCO is decreased
10. Cor pulmonale rare.
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CHRONIC BRONCHITISEMPHYSEMA
BLUE BLOTTERPINK PUFFER
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ALPHA1ANTITRYPSINEMPHYSEMA
Specific circumstances of Alpha 1- ATinclude. 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. MMA1AT 100%
2. MSA1AT 75%
3. SSA1AT 55%
4. MZA1AT 55%
5. SZA1AT 40%
6. ZZA1AT 8%
A1AT LEVELS
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1. Decreased FEV12. Decreased FVC
3. FEV1 < 80%
4. FEV1 FVC < 70%
5. Post bronchodilator
no change in FEV1
6. PEF is decreased
7. FETis prolonged8. V Max - decreased
CLINICAL SIGNSSPIROMETRY
1. Physical exam may be negative2. Hyper-inflated chest, Barrel chest
3. Wheeze or quite breathing
4. Pursed lip / accessory muscles resp.
5. Peripheral edema
6. Cyanosis, JVP
7. Cachexia
8. Cough, wheeze, dyspnea, sputum
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1. No of cigarettes / day2. No of smoker years
3. Age at starting
4. Time of 1stcigarette
5. Desire to quit
6. Barriers to quit
7. Passive smoking
8. Occupational expo.
9. Domestic pollution
MRC DYSPNOEA SCALEABOUTSMOKING
Grade Degree of breathlessness - related activity0 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 mining2. Cotton dust
3. Cement dust
4. Oil fumes
5. Cadmium fumes
6. Grain dust
Rice millers
Grain handlersFlour millers
OXYGEN COST DIAGRAMOCCUPATIONAL
0 10
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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 FACTORSSUPPORT
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 etiology2. Different prognosis
3. Different therapy
4. Different response
to therapy
5. DD includes
Bronchial Asthma
Bronchiectasis- CSLD
Bronchogenic Ca.
DIFF. Dx. of COPD & ASTHMAWHY 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 IMAGES
CHEST SKIAGRAMS
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CHEST SKIAGRAMS
OF EMPHYSEMA
V P MISMATCH
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V- P MISMATCH
NUCLEOTIDE IMAGING
CHEST SKIAGRAM OF
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CHEST SKIAGRAM OF
CHRONIC BRONCHITIS
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CHEST LATERAL VIEW
CHRONIC BRONCHITIS
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HRCTNORMAL CHEST
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HRCTEMPHYSEMA
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HRCTEMPHYSEMA
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ASSESSMENT OF STABLE
COPD
MANAGEMENT OF COPDR OBJECTIVES
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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
complications7. Reduce mortality
8. Minimize side effects
from treatment
MANAGEMENT OF COPDRx. OBJECTIVES
1.Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
Education
Pharmacologic
Non-pharmacologic
4. Manage exacerbations
ASSESSMENT OF COPDMANAGEMENT
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ASSESSMENT OF COPDMANAGEMENT
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 points2. Epidemiology
3. Risk factors
4. PathogenesisPathol
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. Manageexacerbations
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 +
ASSESSMENT OF COPDMANAGEMENT
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ASSESSMENT OF COPDMANAGEMENT
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. PathogenesisPathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
OTHER INVESTIGATIONSTESTS
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OTHER INVESTIGATIONS
1. Serial spirometry tests2. Pulse Oximetry
3. Alpha1Anti-trypsin levels
4. TLCO5. HRCT
6. ECG
7. ECHO8. Sputum culture
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. PathogenesisPathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
TESTS
NORMAL AND COPDSPIROMETRY
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NORMAL AND COPDSPIROMETRY
0
5
1
4
2
3
Liter
1 65432
FVC
FVC
FEV1
FEV1
Normal
COPD
3.900
5.200
2.350
4.150 80 %
60 %
Normal
COPD
FVCFEV1 FVCFEV1/
Seconds
WITH BRONCHODILATORREVERSIBILITY
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WITH BRONCHODILATORREVERSIBILITY
PROTOCOL
1. Patient must be clinically stable
2. Patient should avoid
Short acting agonists for 6 hours
Long acting agonists 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. PathogenesisPathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
WITH STEROIDSREVERSIBILITY
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WITH STEROIDSREVERSIBILITY
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/day4. 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. PathogenesisPathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
WHAT IS REVERSIBILITY ?TESTING
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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 FEV1must 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. PathogenesisPathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
SEVERITY OF COPDFACTORS
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1. Severity of symptoms
2. Stages of COPD
3. Frequency and severity
of exacerbations
4. Presence of
complications of COPD5. Presence of respiratory
insufficiency
6. Co-morbidity
7. General health status
8. Number of medications
needed to manage the
disease
SEVERITY OF COPDFACTORS
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 REDUCTION
STRATEGIES
IF ONE QUITS SMOKINGNO
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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 SMOKINGNO
TOMORROW!
1. Treatment starts with reducingriskspack 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
5 RELAPSE RISK FACTORS REDUCTION
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5. Withdrawal
4. Boredom
3. Sense of deprivation
or depression
2. Emotional upset andstress
1. Alcohol abuse !
One devil replaced
by another devil
5 RELAPSE
TRIGGERS
1. Exposure to smoking, noxious agn2. 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
NICOTINE REPLACEMENTSDRUG TO QUIT
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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 orseizure disorder
NICOTINE REPLACEMENTSDRUG 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 MANAGEMENT
LATEST GUIDELINES
MANAGEMENT GOALS OF MANAGEMENT
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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
HOW TO OUTCOME MEASURES
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HOW TO
ASSESS?
1. Spirometric assessment2. 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
BRONCHO- MANAGEMENT - IBD
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BRONCHO
DILATORS
IBD are the main stay As when needed basis
The main drugs are
2- 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
MANAGEMENT BUT UNFORTUNATELY
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MANAGEMENT
1. IBD do not alter the pathology2. Drug Rx. is to improve
symptoms andcomplications.
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
THE RULES MANAGEMENT RULES
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THE RULES
1. NO systemic steroids in stable COPD
2. Inhalation treatment is BEST
3. Salmeterol is the FIRST choice
4. Ipatropium is the SECOND choice
5. Salbutamol for short bursts6. Inhaled steroids THIRD choice
7. Combination Ipa + Salmet inhalers beneficial
8. Oral 2Agonists FOURTH choice
9. Theophyllins ? roleLA 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
BRONCHO IS IT A PARADOX ?
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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 FEV1or 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 ?
SYNERGISM BRONCHODILATION
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SYNERGISM BRONCHODILATION
IPATROPIUM SABA and LABA
AGONISTS BRONCHODILATORS
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AGONISTS
1. Direct action on the beta2
receptors in thebronchial smooth musclerelaxation
2. Salbutamol most widely used
3. In COPD 1 mg is the maximum dose
4. Short actingevery 4 to 6 hours5. Salmeterol is long acting12 hours
6. Slow onset, dose 50 g b.i.d
7. Formoterol still longer -12 g b.i.d
8. Side effectstremors, tachycardia etc.,
1. Selective agonists
2. Short acting drugs
3. Long acting drugs
4. Oral medication
5. Inhaled form
BRONCHODILATORS
ANTI ACH BRONCHODILATORS
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ANTI ACH
1. Cholinergic drive is in the bronchii
2. Anti-cholinergicsresting bronchial tone
3. Three muscarinic receptors M1, M2, M3
4. Ipatropium, Oxitropiumonset slower than
agonistsbut more effective5. Sustained broncho-dilatationup to 8 h
6. Have influence on sleep quality in COPD
7. Ipatropium optimal dose 80 g as inhaler
8. Tiotropiumselective to M1, M3 receptors
9. It is long actingonce a daydose 40 g
1. Anti-cholinergics
2. Short acting drugs
3. Long acting drugs
4. Inhaled forms
5. Combination with
beta agonists
BRONCHODILATORS
ORAL CORTICOSTEROIDS
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ORAL
STEROIDS
Inhaled Glucocorticoids
In stage I and II COPDno 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 componentthey 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 ofpatients sustained
improvement
5. Similar to asthmatics
6. Significant risk of sideeffects
CORTICOSTEROIDS
THEOPHYLLIN BRONCHODILATORS
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O N
E
1. Assumed to relax the airway smooth muscle
2. At therapeutic concentration NO direct action
on the bronchial smooth muscle
3. ToxicityMany drug interactions
4. Low therapeutic index - Poor safety window5. Need to monitor blood levels frequently
6. Adverse effects on liver and in elderly
7. Their use is at best questionable
8. Never injectablein 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
INHALED Rx. MANAGEMENT
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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
NO SYSTEMIC MANAGEMENT
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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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MANGEMENT
AS PER STAGING
AT RISK MANAGEMENT - STAGE 0
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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
MILD COPD MANAGEMENTSTAGE I
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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. Spirometryabnormal
7. FEV1 > 80% but
8. FEV1 / FVC < 70%
MODERATE MANAGEMENTSTAGE II
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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%
SEVERE COPD MANAGEMENTSTAGE III
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Avoidance of risk factors
Stop smoking
Influenza vaccine
Regular follow up spirometry
SABA + IPA inhalations +
LABA or TIOTROP or BOTH inhaled
Pulmonary Rehabilitation
ICSBudesonide
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%
V. SEVERE MANAGEMENTSTAGE IV
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COPD
Avoidance of risk factors
Stop smoking
Influenza vaccine
Regular follow up spirometry
SABA + IPA inhalations + LABA or TIOTROP or BOTH inhaled
Pulmonary Rehabilitation
ICSBudesonide
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
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DRUG DELIVERY
SYSTEMS - OPTIONS
DRUG DRUG DELIVERY - OPTIONS
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DELIVERY
MDIMetered Dose Inhalers
Rotahalers, Diskhalers
Spacehalers
Nebulizers Oxygen mixed delivery
Oral tablets, syrups ??
ParenteralI.M or I.V use ????
1. Dexterity
2. Hand grip strength
3. Co-ordination
4. Severity of COPD5. Educational level
6. Age of the patient
7. Ability to inhaleand synchronize
NEBULISED THERAPY
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NEBULISED THERAPY
1. Severe breathlessness despite using inhalers
2. Assessment should be done for improvement
3. Choice between a facemask or mouth piece
4. Equipment servicing and support are essential
5. 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 rate
7. Can be repeated 2 to 3 times a dayMouth Wash
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EDUCATION AND
REHABILITATION
REHABILITATION
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For the lungs to get more air
PURSED-LIP BREATHING(like breathing out slowly into a straw)
INHALE EXHALE
REHABILIT
ATION
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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 youbreathe in)
3. Then push in your
abdominal muscles and
breathe out using the
pursed-lip technique.
(You should feel yourabdomen go down)
Note:
Repeat the above maneuver three times and then take a little rest.
This exercise can be done many times a day.
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
HEALTH EDUCATION TEAM WORK
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HEALTH EDUCATION TEAM WORK
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EXACERBATIONS
RESP. FAILURE
OXIGENERATO MANAGEMENTREFERRAL
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R
Diagnosis uncertain Disproportionate symptoms
Persistent symptoms
Development of lung cancer Pulmonary rehabilitation
Nebulizer assessment
Oxygen assessment
WHEN D.D. of EXACERBATIONS
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SUSPECT?
1. Pulmonary embolism
2. Pneumothoraxrupture of bullae
3. Myocardial infarction
4. Left ventricular failure
5. Acute pneumonia
6. Bronchogenic carcinoma
1. in symptoms
2. in sp purulence
3. in sp volume
4. Fever, chills
5. Ankle edema
6. Cyanosis
7. Consciousness
WHAT EXTRA ? MANAGE EXACERBATIONS
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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 smoking
In 35% of cases cause is not known
3. Systemic corticosteroidsoral better
4. Antibiotics in short burstswhat to give
5. NIPPVNon invasive intermittentpositive 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
antibiotics2 wks
8. Oral steroids for 2 wk
9. Diuretics may help
LONG TERM OXYGEN THERAPYINDICATIONS
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Pulse oximetry to know PaO2
Arterial blood gas saturation monthly
Review LTOT every year
Oxygen concentrators - oxygen cylinders
Fire warningsmoking
Ambulatory oxygen therapyO2 cylinders,
liquid oxygen
SBOT - Short burst OTExacerbations.
NIPPV in patients with respiratory drive
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
CORPULMONALEFEATURES
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LTOT
Diuretics, Sodium restriction
ACEi
Alpha blockers
Digoxin
Heart failure management
1. Increasing dyspnea
2. Peripheral oedema
3. venous pressure
4. Parasternal heave
5. Loud pulmonarysecond heart sound
6. ECG changes of RVH
and PH
7. Echo evidence
RESP. FAILURE RESPIRATORY FAILURE
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1. Pulmonary hypertension
2. Right ventricular hypertrophy
3. Right ventricular diastolic dys. function
4. Right ventricular systolic dysfunction
5. CorpulmonaleRight heart failure6. Acute respiratory insufficiency
7. Life threatening respiratory failure
8. Hypercapnia, Severe hypoxia9. Intubation and IPPV
10. Managing RVF and RFICU care
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
4. Education5. Pharmacologic
6. Non-pharmacologic
7. Management of
exacerbations
SURGERY LUNG RESECTION
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1. Increasing dyspnea
2. Single large emphysematous bulla
3. Severe - FEV1 < 35% but > 20%
4. Upper lobe emphysema
5. PaCo2 not more than 55%
6. TLCO must be at least 20%
7. Age less than 65
8. Severe pulmonary hypertension
1. Bullectomy
2. LVRS - Lung volume
reduction surgery
3. Single lung transplant
WHAT NOT ! WHAT ELSE WE CAN GIVE
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Pneumococcal vaccine may be given
Early initiation of O2 shown to survival
Prolonged use of inhaled steroids
long acting better2 weeks duration
Alpha1anti-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 termantibiotics
5. No systemic steroids
6. No narcotics
7. No vigorous exercise
8. No with holding the
benefits of Oxygen
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COPD - FUTURE DEVELOPMENTS
NEXT DECADE FUTURE DEVELOPMENTS
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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 inhibitorsfor bronchodilatation
Drugs toNeutrophilic 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
TAKE HOME MESSAGES
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COPD is no more a specialists concernit is ours !
It is alarmingly increasingIt is preventable
Please differentiate Asthma and COPD
Use spirometry, peak flow meter - just as ECG
Dont embark on Deri + Bet iv for all breathlessness
Dont use Theophylline as far as possible
Inhalation therapy is the bestDrug delivery choices
Dont spare any body from early oxygen therapy
And finally, motivate smokers to quit smoking
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SELF SCREENING
Could it be COPD?
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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 dont 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 haveCOPD 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 lungsLearn about COPD!
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ASTHMA V/s COPD
Take HOME GUIDE
ASTHMA V/s COPD
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ASTHMA 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
ASTHMA V/s COPD
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ASTHMA 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
ASTHMA V/s COPD
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ASTHMA 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-PATHOGENESIS
ASTHMA V/s COPD
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ASTHMA 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 dyspneamoder. Progressive dyspn, Hr. Gr.
Seasonal symptoms Perennial symptoms
CLINICAL FEATURES
ASTHMA V/s COPD
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ASTHMA 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
ASTHMA V/s COPD. - Rx.
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Dr.Sarma@works110Treatment
ASTHMA COPD
Relievers and Preventers Quitting of smoking crucial
ICS are the main stay LABA + AntibioticsAc. 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.
This is most pertinent today to Asthma
and COPD
Tennyson Sir Lord, Alfred
Holm and Harris & NEJM
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PREVENT COPD
THE DEADLIEST DEVIL
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SURE TO GRAVE
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AND FINALLY
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Tell me what harm smoking
does notcause ??
TELL ME THE
ORGAN SPARED
PROVEN DISASTERS
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ORGAN SPARED
1. IHD, MI, Restenosis
2. AtherosclerosisPVD, IR, DM
3. Oxidation of LDL, LDL, HDL, TG
4. COPD, Lung Cancer
5. Tremors, Peripheral neuritis6. APD, NUD, Oro-pharyngeal Cancers
7. Osteoporosis
8. Poor fetal development
9. Nicotine dependence
10. 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 utero9. The psyche
10.The Purse
The Onus here is on us
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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 riskinverse response.
If we are a smoker, let us quit smokingset an example.
Let us motivate every month at least one person to quit.
What right we have, to make others passive smokers?
Pledge to stop smoking
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WHAT CAN WE DO ??
MY SINS IF CARE NOT TO DO
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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 haveSINS
PUNYAS
THESETHEN ALL
MY GAINS HAVE NO MEANING &
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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 K9. My rituals
ARE MERELY FUTILE
SINS
PUNYAS
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122Dr.Sarma@works
REMEMBER, WE ARE BLESSED
WITH THE OPPORTUNITY
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Om Asatho maa sad gamayaOm Tamaso maa jyothir gamaya
Om Mrityor maa amritam gamaya
Om Sarveshaam swasthir bhavathu
Om Sarveshaam shaantir bhavathu
Om Shaantihi Shaantihi Shaantihi ||
Important Announcement
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A CD format of todays presentation is ready
1. COPD, Asthma and basics of spirometry
In addition it, also contains2. ECG workshop presented earlier
3. Guidelines on Hypertension treatment
This can be used in Computer & DVD player
Resources for
COPD and Asthma
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1. ACCP www.chestnet.org
2. ATS www.thoracic.org
3. BTS www.brit-thoracic.org.uk
4. COPD profess. www.copdprofessional.com
5. GOLD www.goldcopd.com
6. NICE www.nice.uk.org
7. Chest Net www.chestnet.net
8. CDC www.cdc.nih.gov
9. NAEPP www.naepp.nhlbi.org
10.COPD Rapid series by ELSEVIER
CO a d st a
PLEASE CONTACT US
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Dr.Sarma@works126
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