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( COPD)
Chronic Obstructive
Pulmonary Disease
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Why COPD is Important ?
COPD is the only chronic disease that isshowing progressive upward trend in bothmortality and morbidity
COPD is the fourth leading cause of deathand affects approximately >16 million
persons in the USA
It is expected to be the third leading causeof death worldwide by 2020
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Definition
Chronic obstructive pulmonary disease (COPD)is a preventable and treatable diseasestatecharacterised by airflow limitation that is not
fully reversible The air f low limitationis usually progressive and
is associated with an abnormal inflammatoryresponseof the lungs to noxious particles or
gases, primarily caused by cigarette smoking
Although COPD affects the lungs, it alsoproduces significant systemic consequences
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Venn diagram of COPD.
Chronic obstructive lung disease is a disorder in which
subsets of patients may have dominant features of chronic
bronchitis, emphysema, or asthma. The result is airflow
obstruction that is not fully reversible.
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Component of COPD
Include:
Emphysema:characterized by destruction and
enlargement of the lung alveoli Chronic bronchitis: with chronic cough andphlegm, with airflow limitation
Small airways disease:a condition in whichsmall bronchioles are narrowed
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Chronic bronchi t isis defined cl inical lyas the presence of a
chronic productive cough for 3 months during each of 2consecutive years (other causes of cough being excluded).
Emphysemais defined pathological lyas an abnormal,permanent enlargement of the air spaces distal to the terminal
bronchioles, accompanied by destruction of their walls and
without obvious fibrosis.
Although some patients predominantly display signs of one of
these diseases or the other, most fall somewhere in the middle
of the spectrum between the 2 conditions.
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Component of COPD
Exclude:
Other causes of chronic airflow obstruction:
Pulmonary cystic fibrosis Diffuse panbronchiolitis
Bronchiectasis
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Risk Factors
Cigarette smoking: a major risk factor for mortalityfrom COPD Airway responsiveness Respiratory infections: childhood and adult
respiratory infections Occupational exposures: coal mining, gold miningand cotton textile dust
Ambient air pollution
Passive or second hand exposure Genetic considerations: 1 antitrypsin deficiency Gender: More common in men
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Pathophysio logy
Patholog ic changesin chronic obstructive pulmonary
disease (COPD) occur in :
the large (central) airways,
the small (peripheral) bronchioles,
the lung parenchyma.
The pathogenic mechanisms are not clear but are mostlikely diverse:
Increased numbers of activated polymorphonuclear leukocytes
macrophages release elastases in a manner that cannot be counteracted
effectively by antiproteases, resulting in lung destruction.
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Pathophysiology
Persistent reduction in forced expiratory flow rates = typical finding
Airflow Limitation( airflow obs. ) and AirTrapping
The inflammation, fibrosis and luminal exudates in small
airways is correlated with the reduction in FEV1 andFEV1/FVC ratio ( spirometry )
The peripheral airway obstruction traps air duringexpiration, resulting in hyperinflation
Emphysema is more associated with gas exchangeabnormalities than with reduced FEV1
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Pathophysiology
Gas Exchange Abnormalities hypoxemia and/or hypercapnia
Mucus Hypersecretion
Pulmonary Hypertension Hypoxic vasoconstriction of small pulmonary arteries eventually
result in structural changes that include intimal hyperplasia and latersmooth muscle hypertrophy/hyperplasia
The loss of the pulmonary capillary bed in emphysema may alsocontribute to increased pressure in the pulmonary circulation
Progressive pulmonary hypertension may lead to right ventricularhypertrophy and eventually to right-side cardiac failure (cor
pulmonale)
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Anatomo Pathology
Pathological changes characteristic of COPD are
found in:
the proximal airways
Distal airways lung parenchyma
and pulmonary vasculature
These changes include chronic inflammation and
structural changes.
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Gross pathology of advanced emphysema. Large
bullae are present on the surface of the lung.
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Pathology
Proximal airways ( trachea, bronchi > 2mm internal diameter)
Goblet cells hiperplasia and enlarged
submucosal glands (both leading to mucushypersecretion)
Squamous metaplasia of epithelium
Smooth-muscle hyperthropy and bronchialhypereactivity
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Pathology
Peripheral airways ( bronchioles < 2 mm internaldiameter)
Goblet cell metaplasia, replacement of surfactant- secretingcells with mucus-secreting and infiltrating cells and smooth-
muscle hypertrophy, these abnormalities may cause:airway wall thickening
peribronchial fibrosis
luminal inflammatory exudate
airway narrowing (obstructive bronchiolitis)
Increased inflammatory response and exudate correlated withdisease severity.
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Chronic bronchi t is
Mucous gland hyperplasia =the histologic hallmarkof chronic bronchitis.
Airway structural changes include :
atrophy,
focal squamous metaplasia,
ciliary abnormalities,
variable amounts of airway smooth muscle hyperplasia,
inflammation,
bronchial wall thickening.
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Histopathology of chronic bronchitis showing hyperplasia ofmucous glands and infiltration of the airway wall with
inflammatory cells.
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Emphysema
Emphysema is a pathologic diagnosis defined by permanentenlargement of airspaces distal to the terminal bronchioles=>
dramatic decline in the alveolar surface area available for gas
exchange =>airflow limitation by 2 mechanisms.
First, loss of the alveolar walls results in a decrease in
elastic recoil =>airflow limitation.
Second, loss of the alveolar supporting structure =>airwaynarrowing, which further limits airflow.
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Emphysema has 3 morpholog ic patterns:
Centriacinar
Panacinar
Distal acinar, or paraseptal
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Pathology
Normal distal lung acinus20
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Pathology
Centriacinar(centrilobular) emphysema21
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Pathology
Panacinar emphysema22
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Pathogenesis
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Pathogenesis
Air f low limitationthe major physiologic change
in COPD, fibrosis is a significant contributor
The pathogenesis :
1.Chronic exposure to cigarette smoke
2. Inflammation and extracellular matrix proteolysis
3.Apoptosis of structural cells of the lung
4. Ineffective repair
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Clinical Manifestation
History of exposure to risk factors Tobacco smoke
Occupational dusts and chemicals
Smoke from home cooking and heating fuel
Age of onset: after middle age
Season: winter
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Clinical Manifestation Most patients with chronic obstructive
pulmonary disease (COPD) seek medicalattention late in the course of their d isease.
Patients often ignore the symptoms because
they start gradually and progress over thecourse of years.
Patients typically present with a combinat ion
of s igns and symptoms o f chron ic
bronchi t is , emphysema, and react ive
airway d isease. 26
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Clinical Manifestation
Symptoms: Dyspnea: gradually progressive dyspnea is the most common presentingcharacter
a.Progressive (worsens over time)
b.Persistent (present every day)
c.Worse on exercised.Worse during respiratory infections
Described by the patient as an increased effort to breathe,heaviness, airhunger or gasping
Chronic cough
Present intermittently or every day often present throughout the day; seldomonly nocturnal
Chronic sputum productionPresent for many years, worst in winters. Initially mucoidbecomes purulent
with exacerbation
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Clinical Manifestation
Recurrent respiratory infection
Recurrent attacks leading to cor pulmonale
heart disease Unexpected weight loss
Decreased food appetite
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Clinical Manifestation
Physical Signs: Earlier period: minimal/nonspecific signs
Advanced Stage:
*Inspection:
Barrel-shaped chest ( hyperinflation )
Accessory respiratory muscle participate
Prolonged expiration during quiet breathing
*Palpation:
Weakened fremitus vocalis
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Clinical Manifestation
*Percussion :
Hyperresonant
Depressed diaphragm
Dimination of the area of absolute cardiac dullness
*Auscultation:
Prolonged expiration
Reduced breath sounds
wheezing during quiet breathing
The heart sounds are best heard over the xiphoid area
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Cli i l if t ti
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Clinical manifestations
Patients with predominant emphysema : pinkpuffers ( thin and noncianotic )
Patients with predominant bronchitis : blue
bloaters ( heavy and cianotic )
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Emphysema character is t icsinclude the
following:
Patients may be very thin with a barrel chest
Patients typically have little or no cough or
expectoration
Breathing may be assisted by pursed lips and
use of accessory respiratory muscles; patients
may adopt the t r ipod si t ting posi t ion
The chest may be hyperresonant, and
wheezing may be heard
Heart sounds are very distant33
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Chronic bron chi t is character is t icsinclude the
following:
Patients may be obese
Frequent cough and expectoration are typical
Use of accessory muscles of respiration is common
Coarse rhonchi and wheezing may be heard on auscultation
Patients may have signs of right heart failure (ie, cor
pulmonale), such as edema and cyanosis
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Laboratory findingsSpirometry
Diagnosis
Assessing severity
Assessing prognosis
Monitoring progression
The hallmark of COPD = airflow
obstruction36
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Laboratory findingsSpirometry
FEV1Forced expired volume in the first
second
FVCTotal 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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COPD classification based on spirometry
GOLDStage
Severity Symtomps Postbronchodilator
FEV1/FVC
Postbronchodilator
FEV1Predicted
O At risk Chronic cough, sputum
production
>0.7 80%
I Mild With or without chronic cough or
sputum production
0.7 80%
IIA Moderate With or without chronic cough or
sputum production
0.7 50%-80%
III Severe With or without chronic cough or
sputum production
0.7 30%-50%
IV Very Severe With or without chronic cough or 0.7
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Laboratory findings
Blood examination:In excerbation or acute infection in airway, leucocytosismay be detected.
Elevated hematocrit => cr.hypoxemia , right ventricular
hypertrophy
Sputum examination: Streptococcus pneumonia
Haemophilus influenzae
Moraxella catarrhalis Klebsiella pneumonia
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Laboratory findings
Blood gas analysis:- Arterial blood gas analysis may reveal
hypoxemia (advanced disease.)
- In patients with severe hypoxemia : low arterial
PO2 and high arterial PCO2.
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Chest X Ray
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Chest X-RayChronic bronchitis
Chest Radiograph (X-
Ray)
Non apparent
abnormalityOr thickened and
increased of the lung
markings are noted
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Chest X-RayEmphysema
Chest findings are also varible
flattend and low diaphragm
Intercostal space becomes widen
A horizontal pattern of ribs
A long thin heart shadow
Decreased markings of lung peripheral vessels
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Chest X-RayEmphysema
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Posteroanterior (PA) and lateral chest radiograph in a patient
with severe chronic obstructive pulmonary disease (COPD).
Hyperinflation, depressed diaphragm, increased retrosternal
space, and hypovascularity of lung parenchyma are
demonstrated.
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Computed Tomography
CT: greater sensitivity and specificity for
emphysema than Chest X-Ray, especially
for the diagnosis of bronchiectasis and
evaluation of bullous disease
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A computed tomography (CT) scan shows hyperlucency due to
diffuse hypovascularity and bullae formation, predominantly in
the upper lobes.
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Diagnosis of COPD
Clinical manifestation Auxiliary examinations Significant importance of Pulmonary
function test
Spirometry should be obtained in allpatients with :
exposure to cigarettes, environmental or
occupational pollutants; presence of cough, sputum production or
dyspnea
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Stage
Stable :
Stable symptoms ofcough and sputum
Gasping and dispnea
are alleviated
Exacerbation:
Gradually progressive coughand sputum
Dyspnea and gasping
Increased purulent sputum
followed by recurrent respiratoryinfection
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Differential Diagnosis of COPD
COPD: 1. Mid-life onset2. Slowly progressing symptoms3. Long history of smoking4. Dispnea during exercise5. Largely irreversible airflow limitation
Asthma: 1. Early onset2. Symptoms vary from day to day3. Symptoms at the night/early morning4. A family history5. Airflow limitation that is largely reversible6. Largely reversible airflow limitation7. Allergy, rhinitis, eczema
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Differential Diagnosis of COPD
Pulmonary carcinoma:Commonly occurs in patients over 40 years oldwith cigarette smokingObvious radiological abnormality
Tuberculosis: Onset at all ages Tuberculosis toxic syndrome Lung infiltrate on chest radiography
Microbiological confirmationSputum examination of positive TB bacterium can
confirms the diagnosis!!!
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Differential Diagnosis of COPD
Bronchiectasis:
1. Large volume of purulent sputum
2. Commonly associated with bacterial infection
3. Coarse crack/clubbing on auscultation
4. Bronchial dilation and bronchial wall thickening on
X-ray /CT
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Complication
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Complication
Chronic respiratory failure
Pneumothorax
Chronic pulmonary heart disease
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Treatment-Stable COPD
Education and smoking cessation
Smoking cessation has the greatest capacity to
influence the natural history of COPD
Control the occupational and
environmental pollution
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T S bl COPD
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Treatment-Stable COPD
Aims ofDrug Therapy
Prevent and control symptoms
Increase exercise capacity
Reduce the frequency and severity ofexacerbations
Improve health status
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Approaches to management
Stage I (mild obstruction):
reduction of risk factors (influenza vaccine);
short-acting bronchodilatorStage II (moderate obstruction):
reduction of risk factors (influenza vaccine);
short-acting bronchodilator
long-acting bronchodilator(s);
cardiopulmonary rehabilitation
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Stage III (severe obstruction): reduction of risk factors (influenza vaccine);
short-acting bronchodilator as needed;
long-acting bronchodilator(s);
cardiopulmonary rehabilitation;
+
inhaled glucocorticoids if repeated exacerbations
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Stage IV (very severe obstruction or moderate obstruction with
evidence of chronic respiratory failure):
reduction of risk factors (influenza vaccine);
short-acting bronchodilator as needed;
long-acting bronchodilator(s);
cardiopulmonary rehabilitation;
inhaled glucocorticoids if repeated exacerbation;
long-term oxygen therapy (if criteria met);
consider surgical options such as LVRS and lung transplantation
T t t St bl COPD
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Treatment- Stable COPD
Drug Therapy
1.Bronchodilators:
bronchodilators are central to the symptomatic
management of COPD
improve emptying of the lungs, reduce dynamic
hyperinflation and improve
exercise performance
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T t t St bl COPD
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Treatment- Stable COPD
Drug Therapy
1.Bronchodilators:Three major classes of bronchodilators:
2 - agonists:
Short acting: Salbutamol & Terbutaline
Long acting : Salmeterol & Formoterol
Anticholinergic agents:
Ipratropium & TiotropiumTheophylline :a weak bronchodilator, whichmay have some anti-inflammatory properties
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T t t St bl COPD
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Treatment- Stable COPD
Drug Therapy
2.Glucocorticoids:
Regular treatment with inhaled glucocorticoids is
appropriate for symptomatic patients with an
FEV1
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Treatment
3. Combination therapy:
Combination therapy of long acting 2-agonists andinhaled corticosteroids show a significant additional
effect on pulmonary function and a reduction insymptoms
Mainly in patients with an FEV1
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Treatment
4.Others: Antioxidant agents
Immunoregulators
Vaccine Alpha-1 antitrypsin augmentation
Mucolytic(mucokinetic,mucoregulator)
agents
Antitussives
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Treatment
Oxygen: >15 h /d Long-term oxygen therapy (LTOT) improves
survival, exercise, sleep and cognitive
performance in patients with respiratoryfailure.
The therapeutic goal is to maintain SaO2 90% and PaO2 60mmHg at sea level and rest
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TreatmentLong-term Oxygen therapy
- LTOT -
Indication:For patients with a PaO255 mmHg orSaO288%,with or without hypercapnia
For patients with a PaO2 of 55~70mmHg or
SaO289% as well as pulmonary hypertension /heart failure / polycythemia (hematocrit >55%)
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Treatment
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Treatment
Manage exacerbation
Identify the cause of exacerbation:
Virus or Bacteria or Other uncertain reasons
Assessment of severity:The proceeding history and disease must beconsidered and comparison is very important
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Treatment
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Treatment
Manage exacerbation
2. Bronchodilators:
Increase dose and times properly
Atomization and inhalation
3. Glucocorticosteroids:
Oral or intravenous glucocorticosteroids arerecommended
30 to 40 mg of oral Prednisolone daily for 7-10days is effective and safe
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Treatment
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Treatment
Manage exacerbation
4. Antibiotics: Respiratory infection is the usual predisposing factor
It is advocated to select antibiotics according to culture ofsputum and drug-sensitivity test
5. Mechanical Ventilation:
Noninvasive mechanical ventilation
Invasive mechanical ventilation
6. Others:
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Treatment
Pulmonary rehabilitation
Nutrition
Surgery:- Bullectomy
- Lung volume reduction surgery
- Lung transplantation
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