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8/14/2019 COPD- chinese teacher
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Chronic ObstructivePulmonary Disease (COPD)
GAO Bao-an MDRespiratory Department,
The First College of Clinical Medical Science,
Three Gorges University
E-mail: [email protected]
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● Master clinical manifestation, diagnosis, and
principal protocols of prophylaxis and treatment
of COPD.
● Be familiar with the pathophysiology of COPD.
● Understand COPD is common and frequently-
occurring disease. Incidence is high, and
complication is serious.
The learner will…
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World’s Top Ten Killers (WHO)World’s Top Ten Killers (WHO)
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World’s Top Ten Killers (WHO)World’s Top Ten Killers (WHO)
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Why COPD is Important ?
• COPD is the only chronic disease that is
showing progressive upward trend in both
mortality and morbidity.
• It is expected to be the third leading
cause of death by 2020
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ⅠDefinition
Chronic obstructive pulmonaryChronic obstructive pulmonary
disease is defined asdisease is defined as
--‘a disease state characterized by the--‘a disease state characterized by the
presence of airflow obstruction due topresence of airflow obstruction due to
chronic bronchitischronic bronchitis or or emphysemaemphysema; the; the
airflow obstruction is generally progressive,airflow obstruction is generally progressive,
may be accompanied by airway hyper-may be accompanied by airway hyper-reactivity, and may be partially reversible’reactivity, and may be partially reversible’
American Thoracic Society 1995/ATS
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◎COPD is the 4th leading cause of death in the United States
(behind heart disease, cancer, and cerebrovascular
disease).
◎ In 2000, the WHO estimated 2.74 million deaths worldwide
from COPD.◎ In 1990, COPD was ranked 12th as a burden of disease;
by 2020 it is projected to rank 5th
◎ Approximately 14 million Indians are currently suffering
from COPD.◎ Approximately 32.8 million Chinese are currently suffering
from COPD.
Ⅱ Epidemiology
The Indian J Chest Dis & Allied Sciences 2001; 43:139-47
ZHONG Nanshan GARD. China
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0
0.5
1.0
1.5
2.0
2.5
3.0
1965 - 1998 1965 - 1998
–59% –64% –35% +163% –7%
CoronaryHeart
Disease
Stroke Other CVD COPD All Other Causes
1965 - 19981965 - 1998 1965 - 1998
Percent Change in Age-Adjusted
Death Rates, U.S., 1965-1998
Proportion of 1965 Rate
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Overall prevalence of COPD in China
1 2 . 1
4 . 9
7 . 8
1 2 . 7
5 . 4
8 . 8
1 2 . 4
5 . 1
8 . 2
02468
1 01 21 4
Male Female Total
p r e v
a l e n c e o f C O
P D ( % )
Urban Rural Total
*
#
* Male VS Female: P <0.01; # Urban VS Rural: P <0.01
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Ⅲ Risk factors for COPD
★Tobacco smoking (most common cause)★Smoke from home cooking and heating fuel
★Occupational dust and chemicals
★Gender: More common in men. M:F ratio is5%:2.7% (in India) and12.4%:5.4% (in
China)
★ Increasing age ★ Others:
Infection, nutrition, socioeconomic status
and deficiency of alpha1 antitrypsin
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Ⅳ Pathology of COPDInflammation of small airway and destruction of alveolar wall
Nonsmoker COPD
cilia
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A
C
B
A Hypertrophy of airwaysmooth muscles
B Squamous metaplasia
replace columnar epitheliumfocally
C Enlarged submucosalglands
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Ⅴ Pathogenesis of COPD
1 Abnormal airway inflammation
2 Reactive oxygen species
3 Imbalance of protease-antiprotease
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Cigarette smoke
Alveolar macrophage
Neutrophil
PROTEASES
Alveolar wall destruction(Emphysema) Mucus hypersecretion(Chronic bronchitis)
PROTEASE
INHIBITORS
Neutrophil chemotactic factors
AIRWAY INFLAMMATION OF COPDAIRWAY INFLAMMATION OF COPD
Neutrophil elastaseCathepsins
Matrix metalloproteinases
Cytokines (IL-8, interleukin)Mediators
?CD8 +
lymphocyte
-
Noxious particles or gases
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Mucus secretion
NF-κB
IL-8
Neutrophil
recruitment
TNF-α
a
REACTIVE OXYGEN SPECIES IN COPD
Plasma leak BronchoconstrictionIsoprostanes
ANTIOXIDANTS
Vitamins C and EN -acetyl cysteine
O2-, H202
OH., ONOO-
Anti-proteases
α1-AT
Proteolysis
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Neutrophil elastase
Cathepsins
MMP-1, MMP-9,
MMP12
Granzymes, perforins
Others……..
PROTEASE-ANTIPROTEASE IMBALANCE IN COPDPROTEASE-ANTIPROTEASE IMBALANCE IN COPD
α1-AntitrypsinSLPI
Elafin
TIMPs
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Ⅵ Pathophysiology of COPD
▲ Increased mucus production and reduced mucociliary
clearance
– cough and sputum production
▲ Loss of elastic recoil, Increase smooth muscle tone,Pulmonary hyperinflation
– airway collapse (emphysema)
▲ Gas exchange abnormalities
– hypoxemia and/or hypercapnia (dyspnea, cyanosis) ▲ Pulmonary hypertension: hypoxemia, decreasing capillary
bed
– chronic cor pulmonale (systemic edema)
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Ⅶ Diagnosis of COPD
1 Symptoms
• Cough and mucoid sputum
• Dyspnea-slowlyprogressive
• Wheeze
• Edema (If cor pulmonale)• Winter exacerbations
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Tobacco smokeoccupational dusts and chemical
smoke from home cooking andheating fuel
History of exposure to risk
factors
Repeated episodesAcute bronchitis
Progressive (worsens over time)Persistent (present every day)Worse on exerciseWorse during respiratory infections
Dyspnea that is
Present for many years, worst inwinters. Initially mucous sputumbecomes purulent withexacerbation
Chronic sputum
production
Present intermittently or every dayoften present throughout the day;seldom only nocturnal
Chronic cough
Key indicators for COPD diagnosis
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2 Signs
• barrel chest(hyperinflation)
• Low, flat diaphragm
• Decreased expansion
chest
• Diminished breath
sound, prolonged
expiration, or wheeze• cyanosis
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3 Assistant examination
Chest imaging: Chest x-ray plate, Computer
Tomograph scan
Pulmonary function testing
Other exam: blood routine test, electrocardio-
graph, arterial gas analysis, sputum culture,
etc.
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COPD(emphysema)
Normal
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Normal
CO
PD
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Pulmonary function testing
Spirometry
• Diagnosis
• Assessing severity
• Assessing prognosis
• Monitoring progression
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• FEV1 – Forced expired volume in the
first second• FVC – Total volume of air that can be
exhaled from maximal inhalation to
maximal exhalation• FEV1 /FVC% – The ratio of FEV1 to
FVC, expressed as a percentage.
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Arterial blood gas analysis
In the early stages, mild or moderate hypoxemia (PaO2
60mmHg) without﹤ hypercapnia.
As the disease progresses, hypoxemia becomes more
severe and hypercapnia (PaCO2﹥50mmHg) happens.
Hypercapnia occurs with increasing frequency as the
FEV1 falls below 1 L.
Blood gas abnormalities worsen during acute
exacerbations and may worsen during exercise andsleep.
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4 COPD classification based on Spirometry
<30< 70Very severe
(4 stage)
30-50< 70Severe (3 stage)
50-80< 70Moderate
(2 stage)
>80<70Mild (1 stage)
>80>70At risk (0 stage)
Post bronchodilator
FEV1% predicted
Post bronchodilator
FEV1 /FVC %
Severity
SPIROMETRY is not to substitute for clinical judgment in the
evaluation of the severity of disease in individual patients.
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5 Relationship between COPD and chronic
bronchitis, emphysema, asthma.
Chronic bronchitis is characterized by
‘chronic productive cough for at least 3 months
in each of 2 successive years for which other
causes, such as infection with tuberculosis,
carcinoma of the lung, or chronic heart failure,
have been excluded.
Two types: simple type and wheezing typeThree stages: acute attack phase, chronic
procrastinate phase, and clinical remission
stage.
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Emphysema is characterized by
abnormal permanent enlargement of the
airspaces distal to the terminal bronchioles with
destruction of their walls and without obvious
fibrosis. Destruction is defined as irregular
enlargement of respiratory airspaces; the orderlyappearance of the acinus and its components is
disturbed and may be lost.
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Asthma is characterized by airway inflammation that is manifested by
airway hyper-responsiveness to a variety of
stimuli and by airway obstruction that is
reversible spontaneously or in response totreatment; reversibility may be incomplete in
some patients.
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Asthma
COPD
Bronchitis
Emphysema
Relationship between COPD and chronicbronchitis, emphysema, asthma.
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Ⅷ Differential diagnosis
Low fever, night sweat, loss weight, cough, hemoptysis.
Tuberculin skin test (PPD, purified protein derivative)
(+ ).
bacterium test (+ )(sputum smear or culture). X ray plate
shows special manifestations. Spirometry is normal.
Tuberculosis
Chronic cough, large pyoid sputum in the morning on
arising especially. Persistent middle-large crackles.
Finger clubbing, CT shows dilated airway (tram lines,
signet ring appearance, and grapelike cluster)
Bronchiectasis
Heart diseases history (hypertension, angina, rheumaticvalvular disease). Dyspnea and edema. Small crackles of
low lung. No airflow obstruction. Enlarged heart (X ray).
Heart failure
Family history. Onset from children. Expiratory dyspnea
(cough) in night or morning especially. Allergic symptoms
(rhinitis, eczema). Airflow obstruction is fully reversible.
Asthma
Smoking (occupational ) history. Onset after middle age.
chronic cough, sputum, dyspnea. Symptoms develop
slowly. Airflow obstruction is not reversible fully .
COPD
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Finger clubbing
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grapelike cluster
signet ring appearance
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Ⅸ Prognosis and Course
Disease Course of a Patients with COPD
Symptoms
Exacerbations
Exacerbations
Exacerbation
s
Deterioration
End of Life
FEV1 < 0.75L
mortality rate is 30% at 1 year
mortality rate is 95% at 10 year
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1 general therapy
⊙ Smoking cessation; ⊙ physical activity;
⊙ nutrition; ⊙ oxygen therapy.
2 pharmacotherapy for stable COPD
⊙ bronchodilators; expectorant; antioxidants;⊙ ⊙ ⊙
corticosteroid (some patients need); surgery⊙
3 therapy for exacerbation (acute attack) ⊙ antibiotics; bronchodilators; controlled oxygen;⊙ ⊙
⊙corticosteroid; mechanical ventilation;⊙
⊙
treat complications (pneumothorax, heart failure, etc)
Ⅹ Treatment of COPD
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0
1
2
3
4
5
10 15 20 25 30 35 40 45 50 55 60 65 70 75 80
Age (Years)
F E V 1 ( l i t e r s )
smokingsmoking
StopStop
Smoking cessation
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• Stops accelerated decline in FEV1
• Improves possibility of oxygen therapy benefits
• 3-6 months after quitting: end of cough/phlegmproduction
• 1 year: lung function increased 30mls• 1 year: risk of Small Cell Lung Cancer halved
• 5 years: risk of any lung cancer halved – No progression of COPD
– Sporting performance enhanced
• Methods of smoking cessation – Counseling; Nicotine replacement; Behavior
modification
Smoking cessation
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Physical activity
● Walk, jogging
(30 minutes for at least twice a week )
● pursed-lip breathing● Abdominal breathing
● Qi gong, or Indian yoga
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Nutrition
Low BMI, high mortality
BMI (body mass index)= weight (kg)/high2(m2)
BMI 21 kg/m﹤ 2, mortality rise
Respiratory quotient (RQ)
Protein: 0.8
Fat: 0.71Carbohydrate: 1.0
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Oxygen therapy Long-term O 2 therapy prolongs life in hypoxemic
COPD patients. It needs more than 15 hours a day.
criteria: PaO2 ≤55 mmHg (SaO2,arterial saturation
<= 88%).
O2 is administered by nasal cannula at a flow
rate sufficient to achieve a PaO2 = 60
mmHg (SaO2
= 90%), usually ≤ 3 L/min
with the patient at rest.
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Expectorants★ammonium chloride
0.3-0.6, tid, po.
★bromhexine
16mg, tid, po.★ambroxol
30mg, tid, po.
★gelomyrtol300mg, tid, po.
★T.C.M.
Antioxidants☆Vitamine C
0.1-0.3, tid, po.
☆Vitamine E
0.1-0.2, tid, po.
☆N-acetyl cysteine
0.2, tid or 0.6, qd
☆T.C.M
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Bronchodilators• Short-acting β2-agonist –
Salbutamol • Long-acting β2-agonist -
Salmeterol and Formoterol
• Anticholinergics –
Ipratropium, Tiiotropium• Methylxanthines –
Theophylline, Aminophylline
Steroids• Oral – Prednisone
• Inhaled - Fluticasone,
Budesonide
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Management based on GOLD
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Surgery
Lung volume reduction surgery:
thoracoscope
Lung transplantation:
Single-lung
Double-lung
Th f b ti
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Therapy for exacerbation
(acute attack)
(1)Antibiotics (common G-)bacteria: hemophilus influenza, pseudomonas
cef , Imipenem, Amikacine, etcⅢ
(2)BronchodilatorsSalmeterol , 200ug, q6h-q12h, inhaling
Aminophylline, 0.25, iv drop, Bid
(3)CorticosteroidMethiprednisone 40mg-80mg, iv drop Qd
Dexamethsone 10mg, iv drop Qd
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(4) Controlled oxygen:
O2 is administered by nasal cannula at a flowrate sufficient to achieve a PaO2 ≈ 60mmHg
(SaO2≈90%), usually ≤ 3 L/min.
(5)Mechanical ventilation (respiratory failure)
Noninvasive positive pressure ventilation
Bi-PAP (Bilevel positive airway pressure)
Invasive positive pressure ventilation
( usually nasotracheal intubation )
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Nasal/face mask
NIPPV: BiPAP
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nasotracheal intubation
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