高宝安外国学生copd- chinese teacher

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]



● 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…



World’s Top Ten Killers (WHO)World’s Top Ten Killers (WHO)



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



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



◎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



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



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



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



Ⅳ Pathology of COPDInflammation of small airway and destruction of alveolar wall

Nonsmoker COPD

cilia



A

C

B

A Hypertrophy of airwaysmooth muscles

B Squamous metaplasia

replace columnar epitheliumfocally

C Enlarged submucosalglands



Ⅴ Pathogenesis of COPD

1 Abnormal airway inflammation

2 Reactive oxygen species

3 Imbalance of protease-antiprotease



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



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



Neutrophil elastase

Cathepsins

MMP-1, MMP-9,

MMP12

Granzymes, perforins

Others……..

PROTEASE-ANTIPROTEASE IMBALANCE IN COPDPROTEASE-ANTIPROTEASE IMBALANCE IN COPD

α1-AntitrypsinSLPI

Elafin

TIMPs



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)



Ⅶ Diagnosis of COPD

1 Symptoms

• Cough and mucoid sputum

• Dyspnea-slowlyprogressive

• Wheeze

• Edema (If cor pulmonale)• Winter exacerbations



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



2 Signs

• barrel chest(hyperinflation)

• Low, flat diaphragm

• Decreased expansion

chest

• Diminished breath

sound, prolonged

expiration, or wheeze• cyanosis



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.



COPD(emphysema)

Normal



Normal

CO

PD



Pulmonary function testing

Spirometry

• Diagnosis

• Assessing severity

• Assessing prognosis

• Monitoring progression



• 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.



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.



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.



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.



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.



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.



Asthma

COPD

Bronchitis

Emphysema

Relationship between COPD and chronicbronchitis, emphysema, asthma.



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



Finger clubbing



grapelike cluster

signet ring appearance



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



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



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



• 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



Physical activity

● Walk, jogging

(30 minutes for at least twice a week )

● pursed-lip breathing● Abdominal breathing

● Qi gong, or Indian yoga



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



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.



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



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



Management based on GOLD



Surgery

Lung volume reduction surgery:

thoracoscope

Lung transplantation:

Single-lung

Double-lung

Th f b ti



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



(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 ）



Nasal/face mask

NIPPV: BiPAP

http://www.dxy.cn/bbs/upload/2004/10/03/12532457.jpg



nasotracheal intubation




高宝安外国学生copd- chinese teacher

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