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COPD by Dr Sarma - PowerPoint

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COPD by Dr Sarma - PowerPoint Powered By Docstoc
					             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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  GOLD                 GLOBAL INITIATIVE
                               FOR CHRONIC
                       OBSTRUCTIVE
                       LUNG
                       DISEASE

           NHLBI AND WHO COLLABORATIVE INITIATIVE
                                                    2
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             WORLD COPD DAY
         November 19, EVERY YEAR




        Raising COPD Awareness Worldwide
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   RELEVANCE               PURPOSE OF THIS TALK

1. COPD is very           Present the
   common
2. COPD is often covert     Global strategy
3. COPD is treatable          for the Diagnosis,
4. Culprit is smoking           Management and
5. Symptoms + DD                  Prevention of COPD
   Use spirometry
                                (updated Nov 2004)
6. GP must know to Dx.
   Tests, Rx. and refer    BASED ON THE GOLD, NICE
7. New advances in Rx.         NAEPP, CDC, BTS,
                                 GUIDELINES
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                 DEFINITIONS



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     CONTENTS                       DEFINITION OF COPD

1. Definition - Key points   1. It is chronic
2. Epidemiology              2. It is progressive
3. Risk factors
                             3. Mostly fixed airway obstruction
4. Pathogenesis –Pathol
                             4. Non reversible by bronchodilators
5. Clinical features
                             5. Exposure to noxious agent is a must
6. Diagnosis, Spirometry
7. Antismoking strateg.
                             6. Chronic obstructive lung disease (COLD)
8. Management Guide          7. Chronic obstru. airways disease (COAD)
9. Drug delivery options     8. Two entities in COPD – namely
10.Rehabilitation, Exace.        1. Chronic Bronchitis 2. Emphysema
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2. EMPHYSEMA                    1. CHRONIC BRONCHITIS

1. Alveolar wall            1. Productive cough
   destruction
                            2. For a period of 3 months
2. Irreversible
   enlargement of           3. In each of 2 consecutive years
   the air spaces           4. Absence of any other identifiable
3. Distal to the terminal      cause of excessive sputum production
   bronchioles
                            5. Airflow limitation that is not fully reversible
4. Without evidence
   of fibrosis              6. Abnormal inflammatory response to
                               noxious agent - like smoking



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     CONTENTS                      DEFINITION OF COPD

1. Definition - Key points   ROAD – Recurrent Obstructive Airways Disease
2. Epidemiology              • Bronchial Asthma
3. Risk factors              • Seasonal, Recurrent
4. Pathogenesis –Pathol      • Sensitizing Agent, Other Atopic disorders
5. Clinical features         • Reversible obstruction, Inflammation
6. Diagnosis, Spirometry     COLD – Irreversible, Chronic, Noxious agent
7. Stop smoking strateg.     • Chronic Bronchitis
8. Management Guide          • Emphysema
9. Drug delivery options     • Combination of both
10.Rehabilitation, Exace.
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                  OBSTRUCTIVE LUNG DISEASES

                        ASTHMA




        EMPHYSEMA                                          CHRONIC
                                                          BRONCHITIS




                 FULL                                          NONE
                         REVERSIBILITY OF AIR WAY OBSTRUTION

          ASTHMA                                               COPD
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                 EPIDEMIOLGY
                   OF COPD



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     CONTENTS                             KEY POINTS

1. Definition - Key points   • Underestimated, often covert
2. Epidemiology
                             • It is not diagnosed until clinically overt
3. Risk factors
                             • By that time it is moderately advanced.
4. Pathogenesis –Pathol
5. Clinical features         • The global burden of COPD will increase
6. Diagnosis, Spirometry     • Toll from ↑ tobacco use in alarming
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
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   MORTALITY                     BURDEN OF ILLNESS

Cause            Deaths    • COPD is the 4th leading cause of
                             death (next to IHD, Cancer, CVA).
CHD              724,269
                           • In 2000, the WHO estimated 2.74
Cancer           534,947
                             million COPD deaths worldwide.
CVA              158,060
                           • In 1990, COPD was ranked 12th
COPD             114,318     among the burden of diseases
Accidents         94,828   • By 2020 it is projected to rank 5th.
Diabetes          64,574   • Often, COPD is covert

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  MORTALITY                      COPD PREVALENCE 2000
TRENDS 1965 - 2000

Cause            % Change      Established Market Economies    6.98
                               Formerly Socialist Economies    7.35
CHD                 - 59%      India                           4.38
Cancer              - 64%      China                          26.20
                               Other Asia and Islands          2.89
CVA                 - 39%      Sub-Saharan Africa              4.41
COPD               + 163%      Latin America and Caribbean      3.36
                               Middle Eastern Crescent         2.69
Accident            + 32%      World                           9.34
All other            - 7%   *From Murray & Lopez, 2001



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    MORBIDITY                           WHAT IS WRONG ?

Year       Consultations        • Cigarette smoking is the primary cause.
                                • USA - 47.2 million smoke, ♂ 28%, ♀ 23%
1980              6.1 million
                                • WHO estimates 1.1 B smokers in world.
1985              7.4 million   • This increases to 1.6 billion by 2025.

1990             10.1 million   • Many countries, rates are ↑ alarmingly.
                                • In India, 4,00,000 premature deaths
1995             11.8 million     annually to use of biomass fuels, like
                                  cow dung cakes, open fires
2000             13.9 million
                                • Indoor air pollution, Industrial pollution
2010               ↑↑↑↑           are the major risk factors in our country.


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           SMOKING - THE CULPRIT



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MOST IMP RISK       RISK FACTORS FOR COPD

                 • 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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                 INTENSE CAUSE FOR CONCERN ?


                                 COLLEGE STUDENTS




   TENDER AGE GROUPS

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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



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     CONTENTS                   PATHOGENESIS

1. Definition - Key points       NOXIOUS AGENT
2. Epidemiology              (tobacco smoke, pollutants,
3. Risk factors                occupational exposures
4. Pathogenesis –Pathol                    Genetic factors
5. Clinical features                       Respiratory
6. Diagnosis, Spirometry                   infection
7. Stop smoking strateg.                   Others
8. Management Guide
9. Drug delivery options
                                      COPD
10.Rehabilitation, Exace.
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                      PATHOGENESIS

1. Definition -key
   points
2. Burden of COPD
3. Classification
4. Risk factors
5. Pathogenesis,
6. Pathophysiology,
7. Management
8. Future research



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                        PATHOGENESIS

1. Definition -key
   points
2. Burden of COPD
                      ATOPY
3. Classification
4. Risk factors
5. Pathogenesis,
6. Pathophysiology,
7. Management
8. Future research



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                  SHIFT IN THE DELICATE BALANCE


   Nutrophil elastase                Alpha 1 Anti-trypsin
   Cathepsisns                       SLP 1, Elastin, TIMPs
   MMP-1, MMP- 9, MMP – 12
   Granzymes
   Perforins




        PROTEASES                         ANTI PROTEASES

                             COPD
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     CONTENTS                             PATHOLOGY

1. Definition - Key points   • Irreversible – COPD – Why ?
2. Epidemiology                  – Fibrosis and narrowing of the airways
                                 – Loss of elastic recoil due to alveolar
3. Risk factors                    destruction
4. Pathogenesis –Pathol          – Destruction of alveolar support that
5. Clinical features               maintains patency of small airways
                             • Reversible – Bronchial Asthma
6. Diagnosis, Spirometry
                                 – Accumulation of inflammatory cells,
7. Stop smoking strateg.           mucus, and exudates in bronchi
8. Management Guide              – Smooth muscle contraction in peripheral
                                   and central airways
9. Drug delivery options
                                 – Dynamic hyperinflation during exercise
10.Rehabilitation, Exace.
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                    PATHOLOGY in COPD

                        COPD




                                   1. Mucus gland hypertrophy
                                   2. Smooth muscle hypertrophy
                                   3. Goblet cell hyperplasia
                                   4. Inflammatory infiltrate
   Normal bronchial architecture
                                   5. Excessive mucus
                                                                  26
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     DISSECTING MICROSCOPIC APPEARENCE




             Normal parenchymal   Emphysematous
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                architecture      Lung architecture   27
       ASTHMA                       PATHOLOGY – COPD

1. Eosinophilic inflamm.     1.   Neutrophilic inflammation
2. CD4, Th2 Lymphocyte       2.   Macrophages and CD8 T cells ↑
3. Mast cells                3.   Altered protease/antiprotiase balance
                             4.   Tissue destruction progressive
4. Tissue destruct. less
                             5.   Alpha1 AT↓- Young age emphysema
5. Mainly allergic inflam.
                             6.   Goblet cell size and number ↑ in CB
6. Inflam. Mediators         7.   Inflammatory mediators
    LT D4                         LT B4
    IL 4                          IL 8
    IL 5                          TNF-α


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           PULMONARY HYPERTENSION IN COPD

                              1. Duplication of elastic lamina
                              2. Medial hypertrophy - PH




    Normal Pulmonary Artery
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                 CLINICAL FEATURES



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             EMPHYSEMA                CHRONIC BRONCHITIS
     1.    Severe dyspnea             1.    Mild dyspnea
     2.    Cough after dyspnea        2.    Cough before dyspnea starts
     3.    Scant sputum               3.    Copious, purulent sputum
     4.    Less frequent infections   4.    More frequent infections
     5.    Terminal RF                5.    Repeated resp. insufficiency
     6.    PaCO2 35-40 mmHg           6.    PaCO2 50-60 mmHg
     7.    PaO2 65-75 mmHg            7.    PaO2 45-60 mmHg
     8.    Hematocrit 35-45%          8.    Hematocrit 50-60%
     9.    DLCO is decreased          9.    DLCO is not that much ↓
     10.   Cor pulmonale rare.        10.   Cor pulmonale common

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             EMPHYSEMA     CHRONIC BRONCHITIS




             PINK PUFFER     BLUE BLOTTER
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  EMPHYSEMA           ALPHA1 ANTITRYPSIN ↓

                 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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  A1AT LEVELS        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%



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  SPIROMETRY                         CLINICAL SIGNS

1. Decreased FEV1          1.   Physical exam may be negative
2. Decreased FVC           2.   Hyper-inflated chest, Barrel chest
3. FEV1 < 80%              3.   Wheeze or quite breathing
4. FEV1 ÷ FVC < 70%        4.   Pursed lip / accessory muscles resp.
5. Post bronchodilator –   5.   Peripheral edema
   no change in FEV1
                           6.   Cyanosis, ↑ JVP
6. PEF is decreased
                           7.   Cachexia
7. FET – is prolonged
                           8.   Cough, wheeze, dyspnea, sputum
8. V Max - decreased


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       ABOUT                         MRC DYSPNOEA SCALE
      SMOKING
1. No of cigarettes / day      Grade Degree of breathlessness - related activity
2. No of smoker years            0    No breathlessness except on
                                      strenuous exercise
3. Age at starting
                                 1    Short of breath when walking uphill or
4. Time of   1st   cigarette          while hurrying to catch a bus or train
5. Desire to quit                2    Walks slower than contemporaries or
6. Barriers to quit                   has to stop for breath while walking alone
                                 3    Stops for breath on walking 100 m or
7. Passive smoking
                                      after 2 or 3 minutes continuously
8. Occupational expo.            4    Too breathless to leave house or
9. Domestic pollution                 breathless while dressing


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 OCCUPATIONAL           OXYGEN COST DIAGRAM

1. Coal mining
2. Cotton dust
3. Cement dust
4. Oil fumes
5. Cadmium fumes
6. Grain dust –     0                         10
   Rice millers
   Grain handlers
   Flour millers



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     ‘SUPPORT’                  PROGNOSTIC FACTORS
       STUDY
1. Hypercapnic RF pts.      Several factors affect survival in COPD.
2. 1029 patients studied
                            • Age
3. 89% survived acute
   hospitalization for RF   • Smoking status
4. Only 51% are alive at    • Pulmonary artery pressure
   2 years of follow-up     • Resting heart rate
5. Prognostic factors are   • Airway responsiveness
    • Severity of RF
                            • Hypoxemia
    • Low BMI
                            • Most importantly the level of FEV1
    • Older age
    • Low PaO2/FIO2
                            • Use of long term oxygen therapy


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      WHY D.D              DIFF. Dx. of COPD & ASTHMA
 WITH ASTHMA
             ?
1. Different etiology     Clinical        COPD          ASTHMA
2. Different prognosis    Smoker          Nearly all    May or may not be
3. Different therapy      Age < 35        Rare          Nearly all
4. Different response     Sputum          Productive    Mucoid or none
   to therapy
                          Dyspnea         Persistent    Episodic
5. DD includes
                          Course          Progressive   Variable, static
   Bronchial Asthma
   Bronchiectasis- CSLD   Spirometry      Obstructive   Normal or Obstru.
   Bronchogenic Ca.       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



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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



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Rx. OBJECTIVES                 MANAGEMENT OF COPD

1. Prevent disease         1. Assess and monitor disease
   progression
2. Relieve symptoms        2. Reduce risk factors
3. Improve exercise
   tolerance               3. Manage stable COPD
4. Improve health status         Education
5. Prevent and treat             Pharmacologic
   exacerbations
6. Prevent and treat
                                 Non-pharmacologic
   complications
                           4. Manage exacerbations
7. Reduce mortality
8. Minimize side effects
   from treatment
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 MANAGEMENT                      ASSESSMENT OF COPD

1. Definition - Key points   Diagnosis of COPD is based on
2. Epidemiology
                             1. H/o exposure to noxious agent
3. Risk factors
4. Pathogenesis –Pathol      2. Presence of Air flow limitation
5. Clinical features         3. Non-reversibility of the limitation
6. Diagnosis, Spirometry
                             4. Chronic productive cough
7. Stop smoking strateg.
8. Management Guide          5. Copious sputum, Dyspnea +/-
9. Drug delivery options
10.Rehabilitation, Exace.
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                    ASSESSMENT OF COPD

1. Assess and monitor        Age 35 +
   disease
           SYMPTOMS
2. Reduce risk factors                  EXPOSURE
3. Manage stable COPD
                 COUGH                   SMOKING
4. Education
                 SPUTUM      + or -     OCCUPATION
5. Pharmacologic
                 DYSPNEA                 INDOOR /
6. Non-pharmacologic
                                         OUTDOOR
7. Manage      More than                Air Pollution
              one
   exacerbations month


          SPIROMETRY IS A MUST
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 MANAGEMENT                      ASSESSMENT OF COPD

1. Definition - Key points   Diagnosis of COPD
2. Epidemiology              • Spirometry is the Gold Standard
3. Risk factors
                             • Every COPD suspect must get
4. Pathogenesis –Pathol        spirometry test done
5. Clinical features         • Like ECG, Spirometry is essential
6. Diagnosis, Spirometry
                             • Arterial blood gas tensions are
7. Stop smoking strateg.       needed if the FEV1 < 40%
8. Management Guide
                             • Respiratory failure, Corpulmonale
9. Drug delivery options
10.Rehabilitation, Exace.
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         TESTS                  OTHER INVESTIGATIONS

1. Definition - Key points
                             1. Serial spirometry tests
2. Epidemiology
                             2. Pulse Oximetry
3. Risk factors
                             3. Alpha1 Anti-trypsin levels
4. Pathogenesis –Pathol
                             4. TLCO
5. Clinical features
6. Diagnosis, Spirometry
                             5. HRCT
7. Stop smoking strateg.     6. ECG
8. Management Guide          7. ECHO
9. Drug delivery options     8. Sputum culture
10.Rehabilitation, Exace.
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  SPIROMETRY                          NORMAL AND COPD

           0
                                         FEV1      FVC     FEV1/ FVC
                                Normal   4.150     5.200     80 %
           1                    COPD     2.350     3.900     60 %


           2
                     FEV1
   Liter




           3
                                                       COPD
           4                                                        FVC
                     FEV1

           5                    Normal
                                             FVC
                 1          2     3      4         5       6 Seconds

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REVERSIBILITY                     WITH BRONCHODILATOR
  PROTOCOL
1. Definition - Key points   1.   Patient must be clinically stable
2. Epidemiology              2.   Patient should avoid
                                  Short acting βagonists for 6 hours
3. Risk factors
                                  Long acting βagonists for 12 hours
4. Pathogenesis –Pathol           SR Theophylline for 24 hours
5. Clinical features         3.   Baseline spirometry
6. Diagnosis, Spirometry     4.   Nebulize Salbuamol 2.5 mg + Ipatropium
                                  500mg for 15 minutes with Nacl
7. Stop smoking strateg.
                             5.   Wait for 30 minutes
8. Management Guide          6.   Repeat spirometry
9. Drug delivery options
10.Rehabilitation, Exace.
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REVERSIBILITY                           WITH STEROIDS
  PROTOCOL
1. Definition - Key points   1.   Spirometry before and after steroid
2. Epidemiology              2.   Two weeks treatment with 30 mg
3. Risk factors                   Prednisolone daily or

4. Pathogenesis –Pathol
                             3.   Six weeks treatment with 800 mcg to 1000
                                  mcg of inhaled betamethasone/day
5. Clinical features
                             4.   Results to be interpreted.
6. Diagnosis, Spirometry
                             Look for steroid contraindications
7. Stop smoking strateg.
                             This predicts the COPD group who will benefit
8. Management Guide
                             from inhaled or systemic steroids
9. Drug delivery options
10.Rehabilitation, Exace.
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       TESTING                   WHAT IS REVERSIBILITY ?

1. Definition - Key points   Criteria for reversibility of obstruction
2. Epidemiology              • Spirometry is the Gold Standard
3. Risk factors
                             • Every COPD suspect must get spirometry
4. Pathogenesis –Pathol        test done and reversibility assessed
5. Clinical features         • Post bronchodilator FEV1 must show
6. Diagnosis, Spirometry       increase of at least 200 ml ↑
7. Stop smoking strateg.     • And the increase should be at least
8. Management Guide            15% of the baseline FEV1 value
9. Drug delivery options
10.Rehabilitation, Exace.
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      FACTORS                       SEVERITY OF COPD

1. Severity of symptoms      STAGES OF COPD
2. Stages of COPD             Stage 0   Normal spirometry but with
3. Frequency and severity
                               (At risk) chronic sym. – sputum, dyspnea
   of exacerbations
4. Presence of
                              Stage 1   FEV1 > 80%
   complications of COPD       Mild      FEV1 ÷ FVC is < 70%
5. Presence of respiratory    Stage 2   FEV1 < 80% but > 50%
   insufficiency
                               Moderate FEV1 ÷ FVC is < 60%
6. Co-morbidity
                              Stage 3   FEV1 < 50% but > 30%
7. General health status
                               Severe    FEV1 ÷ FVC is < 40%
8. Number of medications
   needed to manage the       Stage 4   FEV1 < 30%
   disease                     V. severe FEV1 ÷ FVC is < 30%

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                 RISK REDUCTION
                   STRATEGIES



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     NO                         IF ONE QUITS SMOKING
  TOMORROW!
1. Assess and monitor    1. Treatment starts with reducing
   disease                  risks – pack years concept*
2. Reduce risk factors
                         2. Studies have shown that with
3. Manage stable COPD       smoking cessation
4. Education
                            •    The rate of decline in lung
5. Pharmacologic                 function slows
6. Non-pharmacologic        •    There will be definite clinical
7. Manage                        improvement in symptoms
   exacerbations


          * Packets per day x Years of smoking = Pack Years
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     5 RELAPSE              RISK FACTORS REDUCTION
     TRIGGERS
5. Withdrawal             1. ↓Exposure to smoking, noxious agn
4. Boredom
                          2. Smoking cessation is the single most
3. Sense of deprivation
                             effective - and cost effective -
   or depression
                             intervention to reduce the risk of
2. Emotional upset and
   stress                    developing COPD
1. Alcohol abuse !        3. It stops progression of COPD
    One devil replaced
    by another devil




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 DRUG TO QUIT                NICOTINE REPLACEMENTS
      ?
1. Antidepressant -        • Helpful for physical withdrawal symptoms
   Bupropion
                           • Can be dosed according to degree of use
2. In psychological
   dependence on           • Costs the same as daily smoking habit
   nicotine                • Most products of NRT - cautious use in
3. Useful in individuals     cardiac patients
   with or at risk for
   depression–             • Bupropion may be alternative to NRT
4. Contraindicated in      • Nicotex or Smoquit SR 150 b.i.d
   drug interactions or    • Patch is more constant level, sprays &
   seizure disorder
                             inhaler a more rapid effect

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                 COPD MANAGEMENT
                 LATEST GUIDELINES



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 MANAGEMENT                 GOALS OF MANAGEMENT

1. Stable COPD           • Prevent disease progression
2. Exacerbations
                         • Relieve symptoms
3. Respiratory failure
                         • Improve exercise tolerance
4. Cardiac failure
                         • Improve health status
                         • Prevent and treat complications
                         • Prevent and treat exacerbations
                         • Reduce mortality



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       HOW TO                 OUTCOME MEASURES
       ASSESS?
1. Assess and monitor    1. Spirometric assessment
   disease
2. Reduce risk factors   2. Walking distance
3. Manage stable COPD
                         3. Dyspnea indices
4. Education
5. Pharmacologic         4. Symptom scores
6. Non-pharmacologic
                         5. Exacerbation rates
7. Manage
   exacerbations



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      BRONCHO-                  MANAGEMENT - IBD
      DILATORS

1. Assess and monitor    • IBD are the main stay
   disease
2. Reduce risk factors
                         • As when needed basis
3. Manage stable COPD    • The main drugs are
4. Education                – β2 - Agonists (Salbutamol group)
5. Pharmacologic
                            – Anticholinergics (Ipatropium group)
6. Non-pharmacologic
                            – Their combination
7. Manage
   exacerbations            – ?? Theophylline


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 MANAGEMENT                   BUT UNFORTUNATELY

1. Assess and monitor    1.   IBD do not alter the pathology
   disease
2. Reduce risk factors   2.   Drug Rx. is to improve
3. Manage stable COPD         symptoms and ↓complications.
4. Education             3.   But stopping smoking will halt
5. Pharmacologic
                              COPD
6. Non-pharmacologic
7. Manage
   exacerbations



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    THE RULES                  MANAGEMENT RULES

1. Assess and monitor    1.   NO systemic steroids in stable COPD
   disease               2.   Inhalation treatment is BEST
2. Reduce risk factors   3.   Salmeterol is the FIRST choice
3. Manage stable COPD    4.   Ipatropium is the SECOND choice
4. Education             5.   Salbutamol for short bursts
                         6.   Inhaled steroids THIRD choice
5. Pharmacologic
                         7.   Combination Ipa + Salmet inhalers beneficial
6. Non-pharmacologic
                         8.   Oral β2 Agonists FOURTH choice
7. Manage                9.   Theophyllins ? role – LA preps. No injectables
   exacerbations
                         10. Oxygen therapy for exacerbations and RF


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     BRONCHO                      IS IT A PARADOX ?
     DILATORS
1. Assess and monitor    • Bronchodilators in COPD have been
   disease
                           shown to be ineffective in modifying the
2. Reduce risk factors     long-term decline in lung function which is
3. Manage stable COPD      the hallmark of this disease (Class 1).
4. Education
                         • There will be no ↑ in FEV1 or FEV1 ÷ FVC
5. Pharmacologic
                         • But, ↑ in exercise capacity demonstrated.
6. Non-pharmacologic
                           Ipratropium and Salmeterol have been
7. Manage
   exacerbations           shown to improve COPD clinical status



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   SYNERGISM        BRONCHODILATION




       IPATROPIUM     SABA and LABA
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    ß AGONISTS                   BRONCHODILATORS

1. Selective ß agonists   1. Direct action on the beta2 receptors in the
2. Short acting drugs        bronchial smooth muscle – relaxation
3. Long acting drugs
                          2. Salbutamol most widely used
                          3. In COPD 1 mg is the maximum dose
4. Oral medication
                          4. Short acting – every 4 to 6 hours
5. Inhaled form
                          5. Salmeterol is long acting – 12 hours
                          6. Slow onset, dose 50 μg b.i.d
                          7. Formoterol still longer -12 μg b.i.d
                          8. Side effects – tremors, tachycardia etc.,


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      ANTI ACH                  BRONCHODILATORS

1. Anti-cholinergics    1. ↑ Cholinergic drive is in the bronchii
2. Short acting drugs   2.   Anti-cholinergics ↓resting bronchial tone
3. Long acting drugs    3.   Three muscarinic receptors M1, M2, M3
4. Inhaled forms        4.   Ipatropium, Oxitropium – onset slower than
5. Combination with          ß agonists – but more effective
   beta agonists        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

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       ORAL                           CORTICOSTEROIDS
     STEROIDS
1. Asthmatic component        Inhaled Glucocorticoids
2. Quick recovery from        •   In stage I and II COPD – no role to play
   acute exacerbations        •   Betamethasone, Budisonide, Fluticasone
3. Delays next exacerb.       •   Inhaled steroids are preferable and they
4. Only small number of           reduce the # of episodes of exacerbation
   patients sustained         •   To be used in stage III and stage IV COPD
   improvement
                              •   They are useful in short bursts in acute
5. Similar to asthmatics          exacerbations
6. Significant risk of side   •   In people with significant asthma component
   effects                        they are found useful
                              •   No role for long acting steroid injections

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 THEOPHYLLIN                       BRONCHODILATORS
      E
1. Deriphyllin group       1.   Assumed to relax the airway smooth muscle
2. Nausea, tachycardia     2.   At therapeutic concentration NO direct action
3. Fatal arrhythmias            on the bronchial smooth muscle
4. Interactions with       3.   Toxicity – Many drug interactions
   drugs - Macrolides      4.   Low therapeutic index - Poor safety window
5. Smokers have higher     5.   Need to monitor blood levels frequently
   theophylline toxicity
                           6.   Adverse effects on liver and in elderly
6. Already tachycardiac
                           7.   Their use is at best questionable
7. Only oral - if at all   8.   Never injectable – in may countries banned
                           9.   SR prep has some add on value

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   INHALED Rx.                     MANAGEMENT

1. Assess and monitor    • IBD is the preferred drugs
   disease
2. Reduce risk factors   • LABA + Tiotropium is best
3. Manage stable COPD    • LABA + TIO + ICS for Stage III, IV
4. Education
                         • Combination is better than increasing
5. Pharmacologic
                           individual drugs
6. Non-pharmacologic
7. Manage
   exacerbations



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  NO SYSTEMIC                       MANAGEMENT
   STEROIDS
1. Assess and monitor    • No systemic steroids because of
   disease
                         • unfavorable benefit-to-risk ratio
2. Reduce risk factors
3. Manage stable COPD
                         • Exercise training programs,
4. Education             • LTOT > 15 hours per day for RF
5. Pharmacologic         • LTOT increases survival
6. Non-pharmacologic
7. Manage
   exacerbations



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                  MANGEMENT
                 AS PER STAGING



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       AT RISK            MANAGEMENT - STAGE 0

1. Chronic symptoms    • Avoidance of risk factors
2. Cough
                       • Stop smoking
3. Phlegm
4. Dyspnea
                       • Influenza vaccine
5. H/o smoking         • Regular follow up spirometry
6. Spirometry Normal




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    MILD COPD               MANAGEMENT – STAGE I

1. Chronic symptoms      • Avoidance of risk factors
2. Cough
                         • Stop smoking
3. Phlegm
4. Dyspnea
                         • Influenza vaccine
5. H/o smoking           • Regular follow up spirometry +
6. Spirometry abnormal   • SABA + IPATROP
7. FEV1 > 80% but
                         • Inhaled route
8. FEV1 / FVC < 70%




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     MODERATE                 MANAGEMENT – STAGE II
       COPD
1. Chronic symptoms       •   Avoidance of risk factors
2. Cough                  •   Stop smoking
3. Phlegm                 •   Influenza vaccine
4. Dyspnea                •   Regular follow up spirometry
5. H/o smoking            •   SABA + IPA inhalations +
6. Spirometry abnormal    •   LABA or TIOTROP or BOTH in inhaled
7. FEV1 < 80% but > 50%   •   Pulmonary Rehabilitation
8. FEV1 / FVC < 60%




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 SEVERE COPD                 MANAGEMENT – STAGE III

1. Chronic symptoms       • Avoidance of risk factors
2. Cough                  • Stop smoking
3. Phlegm                 • Influenza vaccine
4. Dyspnea                • Regular follow up spirometry
5. H/o smoking
                          • SABA + IPA inhalations +
6. Spirometry abnormal
                          • LABA or TIOTROP or BOTH inhaled
7. FEV1 < 50% but > 30%
                          • Pulmonary Rehabilitation
8. FEV1 / FVC < 40%
                          • ICS – Budesonide
                          • LTOT at least 15 hours per day

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     V. SEVERE                 MANAGEMENT – STAGE IV
        COPD
1. Chronic symptoms        •   Avoidance of risk factors
2. Cough                   •   Stop smoking
3. Phlegm                  •   Influenza vaccine
                           •   Regular follow up spirometry
4. Dyspnea
                           •   SABA + IPA inhalations +
5. H/o smoking
                           •   LABA or TIOTROP or BOTH inhaled
6. Spirometry abnormal
                           •   Pulmonary Rehabilitation
7. FEV1 < 30%              •   ICS – Budesonide
8. FEV1 / FVC < 30%        •   LTOT at least 15 hours per day
9. Chronic Resp. Failure   •   Oral steroids in short bursts
                           •   Surgical treatments
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                  DRUG DELIVERY
                 SYSTEMS - OPTIONS



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       DRUG               DRUG DELIVERY - OPTIONS
     DELIVERY
1. Dexterity            • MDI – Metered Dose Inhalers
2. Hand grip strength   • Rotahalers, Diskhalers
3. Co-ordination        • Spacehalers
4. Severity of COPD     • Nebulizers
5. Educational level    • Oxygen mixed delivery
6. Age of the patient   • Oral tablets, syrups ??
7. Ability to inhale    • Parenteral – I.M or I.V use ????
   and synchronize

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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 above
           6. 15 minutes and slow or moderate flow rate
           7. Can be repeated 2 to 3 times a day – Mouth Wash
                                                                85
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                 EDUCATION AND
                 REHABILITATION



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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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                              REHABILITATION
                             For the lungs to get more air
                           DIAPHRAGMATIC BREATHING




                                2. Put one hand on your 3. Then push in your
    1. Sit comfortably and      abdomen. Now inhale        abdominal muscles and
    relax your shoulders.       slowly through your        breathe out using the
                                nose. (Push your           pursed-lip technique.
                                abdomen out while you      (You should feel your
    Sit comfortably and                                      Then push in your abdominal
                              Put one hand on your abdomen.abdomen go down)
                                breathe in)
    Note: your shoulders
    relax                    Now inhale slowly through your muscles and breathe out
                             nose. three your abdomen out a little rest.
    • Repeat the above maneuver (Push times and then takeusing the pursed-lip technique
                             while you times a day.
    • This exercise can be done many breathe in)
                                                                                      88
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             HEALTH EDUCATION – TEAM WORK




                                            89
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                 EXACERBATIONS
                  RESP. FAILURE



                                  90
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 OXIGENERATO      MANAGEMENT – REFERRAL
      R
                 • Diagnosis uncertain
                 • Disproportionate symptoms
                 • Persistent symptoms
                 • Development of lung cancer
                 • Pulmonary rehabilitation
                 • Nebulizer assessment
                 • Oxygen assessment


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       WHEN                 D.D. of EXACERBATIONS
     SUSPECT?
1. ↑ in symptoms       1.   Pulmonary embolism
2. ↑ in sp purulence   2.   Pneumothorax – rupture of bullae
3. ↑ in sp volume      3.   Myocardial infarction
4. Fever, chills
                       4.   Left ventricular failure
5. Ankle edema
                       5.   Acute pneumonia
6. Cyanosis
                       6.   Bronchogenic carcinoma
7. ↓ Consciousness




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 WHAT EXTRA ?                    MANAGE EXACERBATIONS

1. Oxygen therapy           1. Exacerbations of symptoms requiring
2. NIPPV mostly or             Rx. are important clinically in COPD.
3. Macha. Ventilation       2.   The most common causes of exacerbation are
                                    Infection of the bronchial tree and
4. Ipatropium inhalation
                                    Air pollution and ↑ in smoking
5. SA - Beta agonists               In 35% of cases cause is not known
6. No theophylline group    3. Systemic corticosteroids – oral better
7. Narrow spectrum          4. Antibiotics in short bursts – what to give
   antibiotics – 2 wks
                            5. NIPPV – Non invasive intermittent
8. Oral steroids for 2 wk
                               positive pressure ventilation - Home
9. Diuretics may help

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  INDICATIONS               LONG TERM OXYGEN THERAPY


1. FEV1 < 30% must      • Pulse oximetry to know PaO2
2. Consider if < 50%    • Arterial blood gas saturation monthly
3. PaO2 < 90%           • Review LTOT every year
4. PaCO2 > 60%          • Oxygen concentrators - oxygen cylinders
5. Cyanosis             • Fire warning – smoking
6. ↑ JVP, Pedal edema   • Ambulatory oxygen therapy – O2 cylinders,
7. Pulmonary HT           liquid oxygen
8. Polycythemia         • SBOT - Short burst OT – Exacerbations.
                        • NIPPV in patients with ↓respiratory drive


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     FEATURES                      CORPULMONALE

1. Increasing dyspnea   •   LTOT
2. Peripheral oedema    •   Diuretics, Sodium restriction
3. ↑ venous pressure    •   ACEi
4. Parasternal heave    •   Alpha blockers
5. Loud pulmonary       •   Digoxin
   second heart sound
                        •   Heart failure management
6. ECG changes of RVH
   and PH
7. Echo evidence



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 RESP. FAILURE                 RESPIRATORY FAILURE

1. Assess and monitor    1.    Pulmonary hypertension
   disease
                         2.    Right ventricular hypertrophy
2. Reduce risk factors
                         3.    Right ventricular diastolic dys. function
3. Manage stable COPD    4.    Right ventricular systolic dysfunction
4. Education             5.    Corpulmonale – Right heart failure
5. Pharmacologic         6.    Acute respiratory insufficiency
6. Non-pharmacologic     7.    Life threatening respiratory failure
7. Management of         8.    Hypercapnia, Severe hypoxia
   exacerbations
                         9.    Intubation and IPPV
                         10.   Managing RVF and RF – ICU care
                                                                       96
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      SURGERY                        LUNG RESECTION

1. Bullectomy               1.   Increasing dyspnea
2. LVRS - Lung volume       2.   Single large emphysematous bulla
   reduction surgery
                            3.   Severe - FEV1 < 35% but > 20%
3. Single lung transplant
                            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


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   WHAT NOT !                WHAT ELSE WE CAN GIVE

1. No Anti-tussives       • Pneumococcal vaccine may be given
2. Mucolytics ??          • Early initiation of O2 shown to ↑ survival
3. No prophylactic        • Prolonged use of inhaled steroids –
   antibiotics              long acting better – 2 weeks duration
4. No long term           • Alpha1 anti-trypsin (Prolastin, Aralast)
   antibiotics
                          • Antibiotics in short bursts for exacerbations
5. No systemic steroids
                          • N-Acetyl cysteine (NAC) is shown useful
6. No narcotics
                          • Immuno-modulators are under trial
7. No vigorous exercise
                          • Calcium and vitamin D supplementation
8. No with holding the
   benefits of Oxygen
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                 COPD - FUTURE
                 DEVELOPMENTS



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 NEXT DECADE                      FUTURE DEVELOPMENTS

1. COPD will increase        •   Emphasis on early diagnosis
2. Mortality will increase   •   Effective anti smoking services
3. Dx. facilities increase   •   COPD will be primary care issue by GP
4. Quit smoking a must
                             •   New drug development for COPD perse
5. Industrial pollution ↑
                             •   Tiotropium takes a center stage
6. Newer drugs
                             •   New M1 and M3 blockers are in line
7. New drug delivery
                             •   PDE4 inhibitors – for bronchodilatation
8. Oxygen Therapy ↑
                             •   Drugs to ↓Neutrophilic inflammation
                             •   Mediator antagonists - ↓inflammation
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                     TAKE HOME MESSAGES

        •   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
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                 SELF SCREENING



                                  102
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                         Could it be 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!
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                 ASTHMA V/s COPD
                 Take HOME GUIDE



                                   104
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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
                                                               105
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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
                                                                   106
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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-α

                        PATHOGENESIS
                                                                107
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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 dyspnea – moder.     Progressive dyspn, Hr. Gr.
   Seasonal symptoms             Perennial symptoms

                     CLINICAL FEATURES                         108
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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                        109
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             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.
                                 Treatment                                  110
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              “The old order changeth
                yielding place to new;
               Lest, one good custom
             should corrupt the world.”
                                      Tennyson Sir Lord, Alfred

          This is most pertinent today to
          Asthma and COPD
                                      Holm and Harris & NEJM
                                                              111
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                 PREVENT COPD



                                112
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                 THE DEADLIEST DEVIL




                                       113
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                 SURE TO GRAVE




                                 114
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                 AND FINALLY




              Tell me what harm
            smoking does not cause
                      ??



                                     115
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 TELL ME THE                   PROVEN DISASTERS
ORGAN SPARED
1. The Heart           1.    IHD, MI, ↑ Restenosis
2. Blood vessels       2.    Atherosclerosis – PVD, IR, ↑ DM
3. Metabolic effects   3.    Oxidation of LDL, ↑ LDL, ↓ HDL, ↑ TG
4. Lungs               4.    COPD, Lung Cancer
5. Nervous system      5.    Tremors, Peripheral neuritis
6. G I tract           6.    APD, NUD, Oro-pharyngeal Cancers
7. Bones               7.    Osteoporosis
8. Fetus in utero      8.    Poor fetal development
9. The psyche
                       9.    Nicotine dependence
                       10.   Wasteful expenditure
10.The Purse
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                 The Onus here is on us

         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?


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                 Pledge to stop smoking




                                          118
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                 WHAT CAN WE DO ??



                                     119
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MY SINS                           IF CARE NOT TO DO
                                  THESE – THEN ALL
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                             PUNYAS
I have not updated my K
                                     SINS
 Not shared what I have
Dr.Sarma@works                                         120
MY GAINS                  HAVE NO MEANING &
                          ARE MERELY FUTILE
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                                 PUNYAS

                            SINS
Dr.Sarma@works                                 121
            REMEMBER, WE ARE BLESSED
                 WITH THE OPPORTUNITY




Dr.Sarma@works                          122
            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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                 Important Announcement

          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

                                                         124
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                      Resources for
                     COPD and Asthma
           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
                                                         125
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                   PLEASE CONTACT US

                 Dr.Sarma RVSN, M.D., M.Sc (Canada)
                 JN Road, Jayanagar, Tiruvallur, TN
                  +91 98940 60593, (4116) 260593


                   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
                                                      126
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                  NANRI,
                 VANAKKAM


                            127
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