Chronic Obstructive Lung Disease

(COPD )
LUNG STRUCTURE
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)
DEFINITION
COPD IS A CHRONIC , SLOWLY PROGRESSIVE DISORDER
CHARACTERISED BY AIRFLOW OBSTRUCTION.
( F E V 1 I S L E S S T H A N 8 0 % O F T H E P R E D I C T E D VA L U E
AND FEV1/FVC < 70%. ) WHICH DOES NOT CHANGE
MARKEDLY OVER SEVERAL MONTHS.

T H E I M PA I R E M E N T O F L U N G F U N C T I O N I S L A R G E L Y
F I X E D ( I R R E V E R S I B L E ) B U T M A Y B E PA R T I A L L Y
R E V E R S I B L E B Y B R O N C H O D I L A T O R T H E R A P Y.

COPD IS UNLIKE ASTHMA, IS NOT FULLY REVERSIBLE

CHRONIC BRONCHITIS

Is defined when a cough and sputum occur on most days for

at least 3 consecutive months for at least 2 successive years
( provided other causes of cough had been excluded).

The 'blue bloaters( Chronic bronchitis ) is characterized by

chronic productive cough, likely to be heavy ( obese) and
cyanotic & develop hypercapnia earlier and may develop
oedema and secondary polycythaemia.
MUCUS PRODUCTION
Normal vs Diseased Bronchi
EMPHYSEMA

Referrred to the pathological process of a permanent

destructive enlargement of the airspaces distal to the
terminal bronchioles.

.
 The 'pink puffers ( Emphysema) is characterized by
chronic cough , are typically thin and breathless, and
maintain a normal PaCO2 ( noncyanotic) at rest until
the late stage of disease. have prominent use of
accessory muscles .
Emphysema
Although pure form of Chronic bronchitis &
Emphysema do exist, there is cosiderable overlap in
the vast majority of patients.

( COPD predominantely Chronic bronchitis or

COPD predominantely Emphysema ).

In practice, these phenotypes often overlap.

 AETIOLOGY OF COPD
•RISK FACTORS FOR DEVELOPMENT OF COPD
• Exposures
• Tobacco smoking.
•Occupation-coal miners .
•Outdoor and indoor air pollution
•Low birth weight-may reduce maximally attained lung function in young adult life
•Lung growth-insults including childhood infections or maternal smoking may affect
growth of lung during childhood, resulting in a lower maximally attained lung
function in adult life
•Infections-recurrent infection may accelerate decline in FEV1. Persistence of
adenovirus in lung tissue may alter local inflammatory response predisposing to
lung damage. HIV infection associated with emphysema

Host factors
• Genetic factors-α1-antiproteinase deficiency
•Airway hyper-reactivity
 ETIOLOGY OF COPD

• A variety of factors appear to increase the risk of developing COPD,but the single most
important cause is cigarette smoking.

• Smoking cause its effect by inducing persistent airway inflammation & causing a direct
imbalance in oxidant\ antioxidant capacity & proteinase/antiproteinase load in the lungs
• Only 15% of smokers likely to develop clinically significant COPD & there is a familial
risks associated with the development of COPD.
• Stopping smoking slows the average rate of the decline in FEV1 from 50 – 70 ml/ year to
30 ml/year (i.e. equal to non-smokers ).
• Susceptibility to cigarette smoke varies but both the dose and duration of smoking
appear to be important, and it is unusual to develop COPD with less than 10 pack years
(1 pack year = 20 cigarettes/day/year).

• Alpha 1-antitrypsin deficiency can cause emphysema in non-smokers but this risk is
increased dramatically in enzyme-deficient patient who smoke. 1–2% of COPD
patients are found to have severe 1AT deficiency as a contributing cause
of COPD,
• COPD will rise from the sixth to the third most common cause of death
worldwide by 2020.
• COPD is the fourth leading cause of death
• Leading causes of death :
• Heart disease
• Cancer
• Cerebrovascular disease (stroke)
• Respiratory diseases (COPD)
• Accidents
• Pneumonia and influenza
• Diabetes
• Suicide
• Nephritis
• Chronic liver disease
• All other causes of death
Pathogenesis of COPD
• Pathogenesis
 Tobacco smoking is the main risk factor for COPD, although other
inhaled noxious particles and gases may contribute.
 In addition to inflammation, an imbalance of proteinases and
antiproteinases in the lungs, and oxidative stress are also important in
the pathogenesis of COPD.

• Pathophysiology
 The different pathogenic mechanisms produce the pathological
changes which, in turn, give rise to the physiological abnormalities in
COPD:
mucous hypersecretion and ciliary dysfunction,
airflow limitation and hyperinflation,
gas exchange abnormalities,
pulmonary hypertension,
systemic effects.
 PATHOPHYSIOLOGY

• COPD has both pulmonary and systemic components .

• An enlargement of mucus-secreting glands and an increased number of goblet cells

in the larger airways contribute to enhanced secretion of airway mucus that
manifests as chronic bronchitis.

• Loss of elastic tissue surrounding the smaller airways, accompanied by

inflammation and fibrosis in the airway wall and mucus accumulation within the
airway lumen, results in airflow limitation, further increased by enhanced
cholinergic tone.

• Premature airway closure leads to gas trapping and hyperinflation, which in turn
decrease pulmonary and chest wall compliance.

• During exercise, the time available for expiration shortens, resulting in progressive
hyperinflation.
• The work of breathing is therefore markedly increased, first on exercise but
then, as the disease advances, at rest.
In the alveolar capillary units the unopposed action of proteases and
oxidants results in destruction of the alveoli and the appearance of
emphysema

. Emphysema may be classified by the pattern of the enlarged airspaces:

centriacinar, panacinar and periacinar.

Bullae form in some individuals.

In COPD there is often "air trapping" (increased residual volume and

increased ratio of residual volume to total lung capacity) and progressive
hyperinflation (increased total lung capacity) late in the disease.

COPD may results in impaired gas exchange and respiratory failure.

Inflammatory cells produce elastase
Destroys connective tissue of alveolar walls

Alpha-1 anti-trypsin (or alpha-1 protease inhibitor) is a

protein produced by the liver that circulates in the
blood and limits the action of elastase
 SYSTEMIC EFFECTS OF COPD

Muscular weakness (cellular changes in skeletal muscles ).

Impaired salt & water excretion leading to peripheral oedema.

Altered fat metabolism contributing to weight loss

Increased prevalence of osteoporosis.

Increased circulating inflammatory markers.

 Pathogenesis of COPD
NOXIOUS AGENT
(tobacco smoke, pollutants, occupational agent)

Genetic factors
Respiratory infection
Other

COPD
 Noxious particles
and gases
Host factors

Lung inflammation
Anti-oxidants Anti-proteinases

Oxidative stress Proteinases

Repair mechanisms

COPD pathology
 CLINICAL FEATURES OF COPD

• Clinical features COPD should be suspected in any patient over

the age of 40 years who presents with symptoms of persistent
cough
sputum production
breathlessness.
Many patients have such symptoms for months or years before
seeking medical attention

• Depending on the presentation important differential diagnoses

include asthma, tuberculosis, bronchiectasis and congestive
cardiac failure.
• Chronic severe asthma may be difficult to distinguish from
COPD.
 CLINICAL FEATURES OF COPD

Cough is usually the first symptom but seldom prompts the patient to consult a
doctor.
It is characteristically accompanied by small amounts of mucoid sputum.
Chronic bronchitis is formally defined when a cough and sputum occur on most days
for at least 3 consecutive months for at least 2 successive years.

Haemoptysis may complicate exacerbations of COPD but should not be attributed

to COPD without thorough investigation.

Breathlessness usually heralds the first presentation to the health professional.

In advanced disease, enquiry should be made as to the presence of oedema (which

may be seen for the first time during an exacerbation) and
morning headaches indicative of hypercapnia.
Physical signs
The presence of pitting oedema should be documented and the
body mass index (BMI) recorded.
Crackles may accompany infection but if persistent raise the
possibility of bronchiectasis.
Finger clubbing is not consistent with COPD and should alert the
physician to potentially more serious pathology.

Two classical phenotypes have been described: 'pink puffers'

and 'blue bloaters'.
The 'pink puffers ( Emphysema) are typically thin and
breathless, and maintain a normal PaCO2 ( noncyanotic) at
rest until the late stage of disease. have prominent use of
accessory muscles,
The 'blue bloaters( Chronic bronchitis ) likely to be
heavy and cyanotic & develop hypercapnia earlier and may
develop oedema and secondary polycythaemia.
In practice, these phenotypes often overlap.
 CLINICAL ABNORMALITIES IN PATIENTS WITH ADVANCED AIRWAY OBSTRUCTION ( COPD )

• A reduction in the length of the trachea palpable above the

sternal notch.
• Tracheal descent during inspiration(tracheal tug)
• Contraction of the sternomastoid and scalene muscles on
inspiration
• Excavation of the suprasternal and supraclavicular fossae
during inspiration,together with indrawing of the costal
margins and intercostal spaces.
• Loss of weight (often stimulates unnecessary investigation)
• Pursed lip breathing– physiological response to decrease air
trapping .
• Central cyanosis
• Flapping tremor and bounding pulse(due to hypercapnia)
• Increased antero-posterior diameter of the chest relative to the
lateral diameter (signs of hyperinflation include a barrel chest ).
• decreased tactile vocal fremitus.
• hyperresonant percussion note
• loss of cardiac & hepatic dullness
• decreased breath sounds; prolonged expiratory phase and
expiratory wheezing. (Rhonchi,especially on forced expiration ).
• Peripheral oedema which may indicate cor pulmonale
• Raised JVP, right ventricular heave, loud pulmonary second sound,
tricuspid regurgitation.
• Advanced disease may be accompanied by systemic wasting, with significant weight loss,
bitemporal wasting, and diffuse loss of subcutaneous adipose tissue.
This syndrome has been associated with both inadequate oral intake and elevated levels of
inflammatory cytokines (TNF-).
Such wasting is an independent poor prognostic factor in COPD.

• Clubbing of the digits is not a sign of COPD, and its presence should alert the clinician to
initiate an investigation for causes of clubbing. In this population, the development of
lung cancer is the most likely explanation for newly developed clubbing
CHRONIC OBSTRUCTIVE PULMONARY DISEASE:
COMPLICATIONS OF COPD
• Pulmonary bullae:
Are thin-walled airspaces created by rupture of alveolar walls. They may be
single or multiple , large or small & tend to be situated subpleurally , Rupture of
subpleural bullae may cause pneumothorax,& occationally bullae increase in
size , compress functioning lung tissue & further embarrass pulmonary
ventilation.
Respiratory failure & cor pulmonale are generally late complications in COPD
patients.
 COPD-INVESTIGATIONS
PULMONARY FUNCTION TESTS

THE DIAGNOSIS OF COPD REQUIRES OBJECTIVE

D E M O N S T R AT I O N O F A I R F L O W O B S T R U C T I O N B Y
S P I R O M E T R Y A N D I S E S TA B L I S H E D W H E N
FEV1 IS LESS THAN 80% OF THE PREDICTED
VA L U E A N D A C C O M PA N I E D B Y F E V 1 / F V C < 7 0 %
NORMAL FEV1 EXCLUDE THE DIAGNOSIS OF COPD
R E V E R S A B I L I T Y T E S T I S N E C E S S O RY TO
D E T E C T A S T H M AT I C C A S E S .
LUNG VOLUMES SHOW AN INCREASE IN TLC & RV
DUE TO GAS TRAPPING
T H E C A R B O N E M O N O X I D E T R A N S F E R FA C T O R &
C O E F F I C I E N T A R E M A R K E D LY R E D U C E D I N
PAT I E N T S W I T H S E V E R E M P H Y S E M A C O M P O N E N T
 Diagnosis of COPD
EXPOSURE TO RISK
SYMPTOMS FACTORS
cough tobacco
sputum occupation
dyspnea indoor/outdoor pollution
è

SPIROMETRY
Measurement of arterial blood gases

should be performed in all patients with sever COPD

( FEV1 less than 40% )

Alveolar underventillation causes a fall in paO2 & often a

perminant increase inpaCO2.

Pulse oximetry may prompt referral for a domiciliary

oxygen assessment if less than 93%.
Haematology

Polycythemia (secondary Polycythemia)may develop, but

should not be assumed to be secondary without
measurement of paO2
Venesection may be considered if the haematocrit is above
0.55

In younger patients with predominantly basal emphysema,

α1- antitrypsin level should be assayed.