Chronic Obstructive

(Pulmonary Diseases (COPD

DR:MIE ALI ALI MOHAMED

 Chronic Obstructive Pulmonary
(Diseases (COPD

A group of pulmonary diseases

characterized by increased
resistance to air flow due to partial
or complete obstruction at any level.
 (l) Chronic Bronchitis

It is persistent productive cough (cough of

sputum) for at least 3 consecutive
. months in at least 2 consecutive years
 l) Chronic Bronchitis)

Causes: Due to chronic

irritation of the bronchial mucosa
by:
1- Cigarette smoking.
2- Atmospheric pollution
3- Chronic inflammation of upper
respiratory tract, tonsils or mouth.
Pathology: Occur in middle-
aged men.
 Chronic Bronchitis( 1)

N/E: Bronchial mucosa appears thick, opaque and

covered by excess mucous.
M/E:
1) Epitheluim:
a- Bronchi:
- Goblet cell hyperplasia and decreased number of
ciliated cells.
- Squamous metaplasia and dysplasia.
b- Brochioles:
Goblet cells metaplasia
 Chronic Bronchitis( 1)

2) Subepithelial Tissue:
chronic inflammatory cell
infiltrations.
Bronchial mucous glands are
hyperplastic, hyperactive with
progressive fibrosis.
 Chronic Bronchitis( 1)

Complications:
1- Centrilobular emphysema.
2- Bronchopneumonia.
3- Bronchogenic carcinoma.
4- Chronic hypoxaemia resulting in persistent
pulmonary vasoconstriction, pulmonary
hypertension and cor pulmonale.
5- Cardiac failure.
 Emphysema( 3)

Permanent dilatation of air spaces distal to the

terminal bronchioles accompanied by
damage of their walls.
i.e. respiratory bronchioles, alveolar ducts and
alveoli (respiratory acinus).
Incidence:
The commonest chronic lung disease. It
occurs more in males from 40-60
years of age.
 Emphysema( 3)

A- Centriacinar (Centrilobular):
It involves respiratory bronchiole (central part of
acinus).
Pathogenesis:
It is related to cigarette smoking and it is explained
by the following theories:
 Elastase - antielastase imbalance theory- 1

Smoking weakens the walls of air

spaces by increasing elastase and
inhibiting antielastase
 :Direct Damage Theory( 2

The walls of air spaces are injured

directly by toxic substances of
cigarette smoking.
 :Chronic Bronchitis theory( 3

a- Smoking recruits neutrophils and

macrophages and stimulates the release of
elastase from them.
b- It increases mucus secretion leading to
mucus plugs which partially obstruct the
bronchi and Terminal bronchioles. During
expiration the air is entrapped and
increases gradually the intraluminal
pressure.
 (3) Emphysema

B- Panacinar( Panlobular):
It involves the whole acinus and occurs more in
old females.
Pathogenesis: Related to inherited
deficiency of antielastase (α 1 antitrypsin) in the
patient's blood. Therefore the action of elastase
secreted from neutrophils and macrophages
becomes unopposed.
 : N/E of emphysema

A- Centriacinar emphysema:
Upper zones of the lung lobes are first affected.
The lungs are moderately enlarged.
The affection is mainly centrally located in the
acinus (RB)
C/S:- Enlarged air spaces, which are seen in
clusters at the center of the lung acinus.
 : N/E of emphysema

B- Panacinar emphysema:
l) Barrel shaped chest:
The chest wall takes a fixed exaggerated inspiration
position:
a- The anteroposterior diameter increases to equal the
transverse. The sternum is pushed forward and
moderate kyphosis occurs.
b- The ribs, costal cartilages and the intercostal spaces
are horizontal.
c- The subcostal angle is wide.
 :N/E of emphysema
2) Lungs:
 Lower zones of lung lobes are first affected.
 The lungs are voluminous and very light.
 They are pale and dry .
 The surface is smooth and presents the
indentations of ribs.
 Lungs have a feathery feeling and pit on pressure
(due to loss of elastic tissue).
 Large bullae project on the surface in the poorly
supported parts (along apices, anterior margin and
free edge of base).
 A bulla is an emphysematous space of more than 1
cm in diameter, it is semitranslucent with paper –
thinned walls.
Centrilobular
emphysema
Centrilobular
emphysema
 Emphysema

M/E:
A) Centrilobular emphysema·
Dilated respiratory bronchioles (R.B.) with normal
A.D. and alveoli.
B) Panacinar emphysema.
l) Alveoli are:
Few in number, increased in size, distorted in
shape.
 Emphysema

2) Interalveolar septa:
 Thin and in advanced stages, alveolar septa
rupture.
 The interalveolar capillaries are compressed by
dilated air spaces.
 Emphysema

Complications:
l) Respiratory system:
Ch. bronchitis.
Interstitial emphysema.
Spontaneous pneumothorax
Respiratory failure.
2) C. V. S.:
pulmonary hypertension and right sided heart
failure.
 Other types of Emphysema

I- Obstructive Hyperinflation (emphysema)

II- Compensatory Hyperinflation
(Emphysema)
III- Senile (Atrophic) hyperintlation
(emphysema)
IV- Interstitial Emphysema:
 Pneumonitis
Inflammation of lung tissue.
Classification
1) Bacteria1:
- Lobar pneumonia.
- Bronchopneumonia.
2) Primary Atypical Peneumonitis
3) Loeffler's Pnueumonia
4) Granuloma
5) Lipid Pneumonia
6) Irradiation Pneumonia
 Lobar Pneumonia

Acute bacterial infection involving at least an entire lobe of

lung (due to streptococcus pneumonia in 95 % of cases)
Incidence:
It predominates in middle-aged males.
Method of infection:
By inhalation. (droplet infection)
 Lobar Pneumonia
Pathogenesis:
1- Exogenous or endogenous pneumococci are
inhaled to reach alveoli.
2- They settle into lower lung lobes and one or both
sides are involved.
3- Micro-organisms in alveoli produce an
inflammatory reaction with fluid exudate.
4- it pass from one alveolus to another through
inter- alveolar pores to involve the whole lobe and
the pleura.
 Lobar Pneumonia

5- The fluid together with the cellular exudate expel

air away from the alveoli producing a firm airless
lobe leading to consolidation (hepatisation) of the
affected lobe.
Pathology:
Sero-fibrinous inflammation of lung that passes in
the following stages.
 Lobar Pneumonia
l) Stage of congestion (1-2 days):
N/E:
1- The involved lobe is:
- Enlarged, dark red and heavy.
- Wet sponge in consistancy.
2- Cut surface: exudes a frothy serous fluids
M/E:
1- Inter-alveolar capillaries are congested
2- Alveoli contain oedema, some air, bacteria and
scattered neutrophils.
 Lobar Pneumonia
2) Stage of red hepatization (2 - 4 days):
N /E:
1-The affected lobe:
- Enlarged, red and heavy.
- firm and airless (like the liver)
2- Cut surface: dry and granular.
3- Serofibrinous pleurisy.
4- Hilar L. N. are enlarged (inflamed).
 Lobar Pneumonia

M/E:
1- Inter-alveolar cappillaries still congested.
2- The alveoli are filled with exudate formed of fibrin
network entangling in its meshes excess
neutrophils, R.B.Cs., few macrophages with
bacteria.
 Lobar Pneumonia
3) Stage of grey Hepatization (4-8 days) :

N/E:
1. Affected lobe:
 Enlarged and grey in colour.
 Firm and airless (like the liver)
2. Cut surface: dry and granular.
3. Fibrinous pleurisy.
4. Hilar lymph nodes are enlarged.
 Lobar Pneumonia
M/E:
1-Inter-alveolar capillaries: less congested.
2- Alveoli contain:
- Fibrin threads in the center (fibrin retracts give a
clear zone adjacent to alv. walls).
-Most inflammatory cells are dead and progressively
disintegrat.
-Most micro-organisms are dead and disappear
-Macrophages increase in number.
3- Fibrinous pleurisy
 Lobar Pneumonia

4) Stage of Resolution (8 - 21 days):

Occur in uncomplicated cases:
- Exudate within the alveoli is gradually liquified by
fibrinolytic enzymes of inflammatory cells. It is
reabsorbed through lymphatics or blood vessels or
removed by macrophages and rarely coughed up.
 Lobar Pneumonia

N/E:
1- The affected lobe:
- The size decrease gradually until it becomes normal with
restoration of the normal color.
- The consistency becomes as wet sponge and is finally
airful.
2- Cut surface: Wet, smooth and exudes a frothy creamy
fluid.
3- Pleurisy resolves.
4- Hilar lymphadenitis disappears.
 Lobar Pneumonia

:M/E
.Mild or no congestion of inter-alveolar capillaries 
The alveoli contain liquified inflammatory 
.exudate and increased number of macrophages
. Lastly the affected lobe appears normal 
Complications of Lobar Pneumonia

1) Pulmonary (in the lung):

 Delayed resolution.
 Fibrosis, Lung abscess and gangrene.
2) Extrapulmonary (outside lungs):
 Spread of infection to pleura

Direct, lymphatic and Blood spread

 Toxaemia.

Clinical course:
7-9 days and terminates by crisis (sudden improvement).
 Bacterial Bronchopneumonia

Acute bacterial infection of the bronchioles and the

surrounding alveoli.
Aetiology:
1) Staphylococcus aureus.
2) Streptococcus pyogens.
3) Pnoumococous.
4) haemophilus influenza
Mode of infection: by inhalation.
 Bacterial Bronchopneumonia

Types:
1) Primary bronchopneumonia:
 Due to 1ry (exogenous) invaders.
 Extremes of age.
2) Secondary bronchopneumonia:
Due to 2ry (endogenous) invaders which
complicate other diseases.
 Bacterial Bronchopneumonia

Pathology
Acute suppurative inflammation of bronchioles and
surrounding alveoli.
N/E:
 Multiple patches of consolidation, distributed
through several lung lobes or one lobe.
 Commonly present in lower lobes (basal) of both
lungs (bilateral)
 They are better felt than seen.
 Bacterial Bronchopneumonia

 They are centered around the bronchioles.

 Cut surface of a patch is slightly elevated, dry,
granular, gery red to yellow and exudes pus on
pressure.
 Areas between the patches are either normal,
collapsed or emphysematous.
 Pleurisy is not a marked feature, as the patches do
not usually contact the pleura.
 Bacterial Bronchopneumonia

M/E:
 Patchy affection of bronchioles and
surrounding alveoli of acute suppurative
bronchiolitis at different stages of
development. .
 The surrounding alveoli are filled with
pus rich in inflammatory cells and pus
cells.
 Interalveolar septa are acutely inflamed.
 Bacterial Bronchopneumonia

Complications:
1. In lung:
 Lung abscess and gangrene.
 Lung fibrosis, leading to pulmonary hypertension and
right-sided head failure.
 Bonchiectasis.
2. In pleura:
Empyema.
 Bacterial Bronchopneumonia

3. Outside the lungs:

a- Spread of infection:
- Direct.
- Lymphatic spread.
- Blood spread.
b- Due to toxaemia:

Clinical course: 2-3 weeks and terminates by lysis.

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