copd by dr sarma

8/13/2019 COPD by Dr Sarma

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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


3. Risk factors




7. Stop smoking strateg.

8. Management Guide




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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


3. Risk factors





8. Management Guide




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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


3. Risk factors





8. Management Guide




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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


3. Risk factors





8. Management Guide




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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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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 +/-


3. Risk factors





8. Management Guide




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1. Assess and monitor

disease



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 +



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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





8. Management Guide



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


2. Epidemiology

3. Risk factors





8. Management Guide



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


2. Epidemiology

3. Risk factors





8. Management Guide



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


2. Epidemiology

3. Risk factors





8. Management Guide



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


2. Epidemiology

3. Risk factors





8. Management Guide



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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disease



4. Education

5. 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


disease



4. Education

5. 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


disease



4. Education

5. 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


disease



4. Education

5. 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


disease



4. Education

5. 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


disease



4. Education

5. 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


disease



4. Education

5. 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


disease



4. Education

5. 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


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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Stop smoking

Influenza vaccine


SABA + IPA inhalations +

LABA or TIOTROP or BOTH inhaled


ICSBudesonide

LTOT at least 15 hours per day

1. Chronic symptoms

2. Cough

3. Phlegm

4. Dyspnea

5. H/o smoking


7. FEV1 < 50% but > 30%

8. FEV1 / FVC < 40%

V. SEVERE MANAGEMENTSTAGE IV


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COPD


Stop smoking

Influenza vaccine


SABA + IPA inhalations + LABA or TIOTROP or BOTH inhaled


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


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


disease



4. Education5. 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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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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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 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

copd by dr sarma

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