Anda di halaman 1dari 6

`

MEDICINE II
1.6E CHRONIC OBSTRUCTIVE PULMONARY DISEASE

COPD
Chronic obstructive pulmonary disease(COPD) is a
preventable and treatable disease with some significant extra
pulmonary effects that may contribute to the severity in
individual patients. Its pulmonary component is characterized
by airflow limitation that is not fully reversible. The airflow
limitation is usually progressive and associated with an
abnormal inflammatory response of the lungs to noxious
particles or gases.

Emphysema

Chronic Bronchitis

Small Airways Disease


PERCENT CHANGE IN AGE-AGJUSTED
DEATH RATES, US., 1965 - 1998

4.

RISK FACTORS FOR COPD


Environmental factors
Congenital factors
Cigarette smoke
Alpha-1-anti trypsin
Occupational
deficiency
exposure (cadium &
silica)
Likely (burden of proof Environmental
Low birth weight
good)
pollution
Airway hyper
Passive smoking
responsiveness
Possible
Adenovirus infection
Genetic disposition
Degree of certainty
Certain

LEADING CAUSE OF DEATH

Non-pharmacologic
Manage exacerbations

Normal nonsmokers lose FEV1 at a rate of about 25 - 35 mL/yr


Among susceptible smokers the rate of FEV1 decline is about
90 mL per year
The heavier the smoking, the steeper the decline in FEV1
The increased rate of decline moves toward normal soon after
smoking cessation

OTHER RISK FACTORS


Airway responsiveness
Respiratory infections ?
Occupational exposures ?
Ambient air pollution
Passive, or Second-Hand Smoking

GENETIC CONSIDERATIONS
Alpha1-antitrypsin deficiency
Encoded by protease Inhibitor (PI) locus
S allele slightly reduced levels
Z allele markedly reduced levels
Caucasian populations
Piz individuals severe deficiency
AIRFLOW LIMITATION

CURRENT FACTS ABOUT COPD


More prevalent than asthma, this debilitating disease affects
about 30 million persons in US
In Philippines, it is estimated that 6.3% of adult population
have COPD
Mirroring cigarette usage trends, COPD related mortality
leveled off in men during past 2 decades but increased
markedly in women
Because advanced COPD leads to extensive use of health
care resources, national financial burden is substantial
( in US exceeds $ 30 billion annually)

1.
2.
3.
4.

1.
2.
3.

4 COMPONENTS OF COPD MANAGEMENT


Reduce risk factors
Assess and monitor disease
Manage stable COPD
Education
Pharmacologic

Increased airways resistance


Reduced recoil
Reduced tethering
Expiratory flow limitation
HYPERINFLATION
Caused by reduced expiratory flow rate, destruction of alveoli,
and short exhalation time.
Hyperinflation of the lungs in COPD occurs because of
progressive destruction of the alveoli, reduced expiratory flow
rate, and the relatively short time of exhalation that COPD
patients experience because of obstruction to airflow.
Cholinergic tone contributes to reduced expiratory flow rate and
inadequate exhalation time.

BEI SAMONTE & REAL YATOT Page 1 of 6

Medicine II

1.6E CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Other complications are the fact that chest wall recoil remains
inward, which results in a threshold load at the start of
inspiration; and the flattened, shortened diaphragm muscle,
which leads to inefficiency in force generation.
Patients work harder to breathe.
The posteroanterior (PA) and lateral chest radiographs shown
here illustrate advanced findings of COPD and hyperinflation.
Chest radiograph changes occur late. The expanded chest,
retrosternal air space, low and flat diaphragm, and decrease in
peripheral vascularity highlight the major radiographic findings.
Hyperinflation is readily apparent.

1.5C END STAGE RENAL DISEASE

PaO2 remains normal until FEV1 is 50% of predicted


Elevated PaCO2 not expected until FEV1 is <25% predicted
Pulmonary hypertension, cor pulmonale, right ventricular failure
with chronic hypoxemia (<55mm Hg)

LARGE AIRWAYS
Mucous gland enlargement
Goblet cell hyperplasia
Cough and mucus
Squamous metaplasia of bronchi
Smooth muscle hypertrophy
Bronchial hyperreactivity

SMALL AIRWAYS
Goblet cell metaplasia
Replacement of surfactant-secreting Clara cells
Luminal narrowing
Decreased alveolar attachments
LUNG PARENCHYMA
COPD: UNDERSTANDING THE DISEASE

EXTRACELLULAR MATRIX PROTEOLYSIS


Neutrophil
Macrophage
Neutrophil elastase
Matrix metalloproteinases

PATHOGENESIS
Airflow limitation
Inflammation
Extracellular Matrix Proteolysis
Cell death
Ineffective repair

Cough
Dyspnea
Sputum

Just Short of Breath OR Could it Be COPD?


Do you cough several times most days?
Do you bring up phlegm or mucus most days?
Do you get out of breath more easily than others your age?
Are you older than 40 years?
Are you a current smoker or an ex-smoker?

SYMPTOMS

DIAGNOSIS

BEI SAMONTE & REAL YATOT Page 2 of 6

Medicine II

1.6E CHRONIC OBSTRUCTIVE PULMONARY DISEASE

symptom
Low risk
More
symptoms
High risk
Less
symptoms
High risk
More
symptoms

GOLD 1-2

<=1

>=2

>=10

C
GOLD 3-4
1.5C END STAGE
RENAL DISEASE

>=2

0-1

<10

>=2

>=2

>=10

CLASSIFICATION BY SEVERITY
STAGE
CHARACTERISTICS
I: Mild
FEV1/FVC < 70%; FEV1 80%
predicted
With or without chronic symptoms
(cough, sputum)
II: Moderate
FEV1/FVC < 70%; 50% FEV1 <
80% predicted
With or without chronic symptoms
III: Severe
FEV1/FVC < 70%; 30% FEV1 <
50% predicted
With or without chronic symptoms
IV: Very Severe
FEV1/FVC < 70%; FEV1 < 30%
predicted or
FEV1< 50% predicted plus chronic
respiratory failure

LABORATORY FINDINGS

ABGs
Oximetry
Hypoxemia
PaCO2> 45mmHg
Elevated Hematocrit
Right ventricular hypertrophy

Bullae

CHEST RADIOGRAPHY

Patient
A

ASSESSMENT OF COPD
Symptoms (CAT or mMRC)
Degree of airflow limitation
Risk of exacerbation
Co-morbidities
COMBINED COPD ASSESSMENT
Characteristic Spirometry Exacerbations
Low risk
GOLD 1-2
<=1
Less

mMRC
0-1

CAT
<10

GOLD 3-4

TREATMENT
Smoking Cessation
Bronchodilators
Anticholinergic Agents
Beta Agonists
Inhaled Glucocorticoids
Parenteral Corticosteroids
Theophylline
Oxygen
Others
MANAGEMENT
REDUCE RISK FACTORS
Three types of counseling are especially effective: practical
counseling, social support as part of treatment, and social
support arranged outside of treatment (Evidence A).
Several effective pharmacotherapies for tobacco dependence
are available (Evidence A), and at least one of these
medications should be added to counseling if necessary and in
the absence of contraindications.
Middle-aged smokers who were able to successfully stop
smoking experienced a significant improvement in the rate of
decline in pulmonary function, returning to annual changes
similar to that of nonsmoking patients; all patients with COPD
should be strongly urged to quit and educated about the
benefits of quitting
Combining pharmacotherapy with traditional supportive
approaches considerably enhances the chances of successful
smoking cessation two principal pharmacologic approaches:
BUPROPION originally developed as an antidepressant
medication, and NICOTINE replacement therapy
BENEFITS OF SMOKING CESSATION
20 MINUTES

Blood pressure drops to normal.

Pulse rate drops to normal.

Body temperature of hands and feet increases to


normal.
8 HOURS

Carbon monoxide level in blood drops to normal.

Oxygen level in blood increases to normal.


24 HOURS

Chance of heart attack decreases.


48 HOURS

Nerve endings start regrowing.

Ability to smell and taste is enhanced.


2 WEEKS TO 3 MONTHS

Circulation improves.

Walking becomes easier.

Lung function increases up to 30%.


1 TO 9 MONTHS

BEI SAMONTE & REAL YATOT Page 3 of 6

Medicine II

1.6E CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Coughing, sinus congestion, fatigue, and shortness


of breath decrease.
Cilia regrow in lungs, increasing ability to handle
mucus, clean the lungs, and reduce infection.
Body's overall energy increases.

1 YEAR

Excess risk of coronary heart disease is half that of a


smoker.
5 YEARS

Lung cancer death rate for average smoker (one


pack a day) decreases by almost half.

Stroke risk is reduced to that of a nonsmoker 5-15


years after quitting.

Risk of cancer of the mouth, throat and esophagus is


half that of a smoker's.
10 YEARS

Lung cancer death rate similar to that of


nonsmokers.

Precancerous cells are replaced.

Risk of cancer of the mouth, throat, esophagus,


bladder, kidney and pancreas decreases.
15 YEARS

Risk of coronary heart disease is that of a


nonsmoker.

All COPD-patients benefit from exercise training programs,


improving with respect to both exercise tolerance and
symptoms of dyspnea and fatigue (Evidence A).
OXYGEN

1.5C END STAGE


RENAL
DISEASE

Only therapy
demonstrated to decrease mortality

Bupoprion
Nicotine Replacement
BRONCHODILATORS
Bronchodilators are prescribed on an as-needed or on a
regular basis to prevent or reduce symptoms.
Regular treatment with long-acting inhaled bronchodilators is
more effective and convenient than treatment with short-acting
bronchodilators, but more expensive. Evidence A new
Combining bronchodilators may improve efficacy and decrease
the risk of side effects compared to increasing the dose of a
single bronchodilator.
INHALED CORTICOSTEROIDS
Regular treatment with inhaled glucocorticosteroids is
appropriate for symptomatic COPD patients with an FEV 1 <
60% predicted (Stages III & IV) and repeated exacerbations
e.g. 3 in the last three years (Evidence A was B)
Mahler et al ARJRCCM 2002;166:1084-91
Jones et al ERJ 2003; 21: 66-73
Calverley et al Lancet 2003;361:449-56
Szafranski et al ERJ 2003;21: 74-81
This treatment has been shown to reduce the frequency of
exacerbations and improve health status (Evidence A new).
3 of these studies, glucocorticosteroid combined with a LABA
was more effective than the individual components
Mahler et al ARJRCCM 2002;166:1084-91
Calverley et al Lancet 2003;361:449-56
Szafranski et al ERJ 2003;21: 74-81

Resting hypoxemia
19 hrs > 12 hrs/day
NON-PHARMACOLOGIC THERAPY
General Medical Care

Influenza vaccine

Pneumococcal vaccine
Pulmonary Rehabilitation
Lung Volume Reduction Surgery
Lung Transplantation

LENGTH OF REHABILITATION PROGRAM


The minimum length of an effective rehab program is 2 months;
the longer the program continues, the more effective the results
(Evidence B)
Behnke et al Respir Med 2000; 94:1184-91
Finnerty et al Chest 2001;119:1705-10
Green et al Thorax 2001;56:143-5

GOALS OF COPD MANAGEMENT


Prevent disease progression
Relieved symptoms
Improved health status
Improved exercise tolerance
Prevent/treat exacerbations
Prevent/treat complications
Reduce mortality
Minimize side effects from treatment

MANAGE STABLE COPD


The overall approach to managing stable COPD should be
characterized by a stepwise increase in the treatment,
depending on the severity of the disease.
For patients with COPD, health education can play a role in
improving skills, ability to cope with illness, and health status.
It is effective in accomplishing certain goals, including smoking
cessation (Evidence A).
RECOMMENDATIONS IN GOLD
Recommendation
Evidence Level
Smoking cessation
A
effect on FEV1
A
pharmacotherapy
Bronchodilator
A
SABA
A
LABA
Inhaled corticosteroids
A
Fev1<50% pred
Exacerbations
A
Rehabilitation
A

ORAL CORTICOSTEROIDS & EXERCISE


Chronic treatment with systemic glucocortico-steroids should
be avoided because of an unfavorable benefit-to-risk ratio
(Evidence A).

BEI SAMONTE & REAL YATOT Page 4 of 6

Medicine II

1.6E CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Long-acting bronchodilator
Regular Ipratropium + long acting beta2-agonist ?
plus high dose inhaled corticosteroid

International Consensus on Definition of COPD Exacerbation

1.5C END STAGE


RENAL
DISEASE

A sustained
worsening of the condition, from the stable

state and beyond normal day-to-day variations


Acute in onset
Necessitates a change in regular medication

International Consensus on Staging of Severity of COPD Exacerbation

Mild = increased need for medication and which patients can


manage in their own normal environment

Moderate = increased need for medication and feel must seek


additional medical assistance

Severe = patients or their caregivers recognize and/or rapid


deterioration of condition, requiring hospitalization
PHARMACOLOGIC THERAPY FOR STABLE COPD
Patient Group
1st Choice
2nd Choice
Alternative
Choice
A
SABA prn or
LABA or LA
Theophylline
SA
anticholinergic
anticholinergic
or SABA prn
prn
and SA
anticholinergic
prn
B
LABA or LA
LABA and LA
SABA prn
anticholinergic
anticholinergic
and/or SA
anticholinergic
prn
C
ICS+LABA
LABA
SABA prn
or
and
and/or
LA
LA
SA
anticholinergic
anticholinergic
anticholinergic
prn
Theophylline
PDE-4 inhibitor
D
ICS+LABA
ICS and LA
SABA prn
or
anticholinergic
and/or
LA
or
SA
anticholinergic
ICS+LABA
anticholinergic
And LA
prn
anticholinergic
Theophylline
or
Carbocysteine
LA
anticholinergic
and LABA
or
LA
anticholinergic
and PDE-4
inhibitor
SUMMARY OF PRACTICAL TX GUIDELINES FOR COPD
All patients
Smoking cessation

Mild dyspnoea/rescue medication


Short-acting beta2-agonist

Persistent/severe dyspnoea
Long acting bronchodilators

Recurrent exacerbations

MANAGEMENT OF COPD EXACERBATION


ACUTE EVENT
Broad spectrum antibiotics can reduce inflammatory response,
duration of symptoms and time to recovery of lung function
initial choice of older and less expensive antibiotic for 10-14
days is reasonable
Oral corticosteroid (prednisolone 30 mg OD) for 2 weeks
Bronchodilators (inhaled anticholinergic + short acting beta
agonist)
Methylxanthines are not beneficial and may be harmful in
acute exacerbations of COPD
Long-term therapy and prevention aimed at decreasing
frequency of exacerbations, reducing ER visits and
hospitalizations
Bronchodilators (inhaled anticholinergic, long acting beta
agonists) can reduce incidence of exacerbations by 33%
37%
Inhaled corticosteroids can reduce # of exacerbations in
severe COPD patients (FEV1 < 50% pred)
Mucolytic (N-acetylcysteine) and immunostimulatory agent
OM-85 BV have been shown to reduce # of exacerbations
but need more evidence
Oxygen
Keep arterial saturation >90%
Causes modest increases in paCO2

MECHANICAL VENTILATORY SUPPORT


Non-invasive positive pressure ventilation(NIPPV)
Respiratory failure
Contraindications:
Cardiovascular instability
Impaired mental status
Copious secretions
Craniofacial abnormalities/trauma
Extreme obesity
Significant burns
Invasive Mechanical Ventilation

INVASIVE VENTILATION
Endotracheal tube
Severe respiratory distress
Life-threatening hypoxemia
Severe hypercapnia and/or acidosis
Mortality

BEI SAMONTE & REAL YATOT Page 5 of 6

Medicine II

1.6E CHRONIC OBSTRUCTIVE PULMONARY DISEASE

17 30% for pxs requiring MV


60% for pxs >65 y.o. admitted to the ICU
COPD AND THE PROBLEM OF RECOGNITION

CLINICAL FEATURES OF ASTHMA & COPD


Features
Asthma
COPD
Age group
All ages
Usually > 40 years
Sex
M=F
M>F
Hx of smoking
Occasional
Frequent
Hx of allergy
Often (+)
Occasionally (+)
Major SSX: Cough,
Episodic, seasonal
Usually daily,
dyspnea
progressive
Inh B2 response
Marked
Fast but minimal
Status when not in
(Almost) normal
Chronic symptoms &
exacerb
activity

1.5C END STAGE RENAL DISEASE

Study on Physicians Awareness of COPD in Philippines (1997)

Out of 237 physicians surveyed on a hypothetical case of


COPD, only 137 (58%) gave a correct diagnosis of COPD

Only 43/137 (31%) would use a spirometer to establish


diagnosis of COPD
ASTHMA OR COPD?

KEY MESSAGES TO PHYSICIANS & PUBLIC


Think COPD
Do spirometry
Reduce risk factors
Manage actively
COPD is preventable and treatable

COPD problem will worsen in the coming years in developing


countries like the Philippines (WHO)

COPD is a preventable and treatable disease

Physicians can make a difference in preventing the worsening


of COPD problem (with early detection and effective treatment)
__________________________________________________________
END OF TRANX

DIFFERENCES & SIMILARITIES BETWEEN ASTHMA & COPD

BEI SAMONTE & REAL YATOT Page 6 of 6