Pathology of COPD 2009

8/14/2019 Pathology of COPD 2009

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DR:MIE ALI ALI MOHAMED

Chronic Obstructive

Pulmonary Diseases (COPD(


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Chronic Obstructive PulmonaryDiseases (COPD(

A group of pulmonary diseases

characterized by increasedresistance to air flow due to partialor complete obstruction at any level.


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(l) Chronic Bronchitis

It is persistent productive cough (cough ofsputum) for at least 3 consecutive

months in at least 2 consecutive years.


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)l) Chronic Bronchitis

Causes:Due to chronic

irritation of the bronchial mucosaby:

1- Cigarette smoking.

2- Atmospheric pollution

3- Chronic inflammation of upperrespiratory tract, tonsils or mouth.

Pathology: Occur in middle-aged men.


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)1(Chronic Bronchitis

N/E: Bronchial mucosa appears thick, opaque andcovered 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


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2) Subepithelial Tissue:chronic inflammatory cell

infiltrations.

Bronchial mucous glands arehyperplastic, hyperactive withprogressive fibrosis.


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Complications:1- Centrilobular emphysema.

2- Bronchopneumonia.

3- Bronchogenic carcinoma.4- Chronic hypoxaemia resulting in persistent

pulmonary vasoconstriction, pulmonaryhypertension and cor pulmonale.

5- Cardiac failure.


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)3(Emphysema

Permanent dilatation of air spaces distal to theterminal bronchioles accompanied bydamage of their walls.

i.e. respiratory bronchioles, alveolar ducts andalveoli (respiratory acinus).

Incidence:

The commonest chronic lung disease. Itoccurs more in males from 40-60years of age.


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)3(Emphysema

A- Centriacinar (Centrilobular):It involves respiratory bronchiole (central part of

acinus).

Pathogenesis:

It is related to cigarette smoking and it is explainedby the following theories:


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11--Elastase - antielastase imbalance theoryElastase - antielastase imbalance theory

Smoking weakens the walls of air

spaces by increasing elastase andinhibiting antielastase


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22((Direct Damage TheoryDirect Damage Theory::

The walls of air spaces are injured

directly by toxic substances ofcigarette smoking.


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33((Chronic Bronchitis theoryChronic Bronchitis theory::

a- Smoking recruits neutrophils andmacrophages and stimulates the release of

elastase from them.b- It increases mucus secretion leading to

mucus plugs which partially obstruct thebronchi and Terminal bronchioles. Duringexpiration the air is entrapped andincreases gradually the intraluminalpressure.


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B- Panacinar( Panlobular):It involves the whole acinus and occurs more in

old females.

Pathogenesis: Related to inheriteddeficiency of antielastase ( 1 antitrypsin) in thepatient's blood. Therefore the action of elastase

secreted from neutrophils and macrophagesbecomes unopposed.

(3) Emphysema(3) Emphysema


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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 theacinus (RB)

C/S:- Enlarged air spaces, which are seen in

clusters at the center of the lung acinus.


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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 andmoderate kyphosis occurs.

b- The ribs, costal cartilages and the intercostal spacesare horizontal.

c- The subcostal angle is wide.


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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).


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Large bullae project on the surface in the poorlysupported parts (along apices, anterior margin andfree edge of base).

A bulla is an emphysematous space of more than 1cm in diameter, it is semitranslucent with paper thinned walls.


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Centrilobularemphysema


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Centrilobular

emphysema


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Emphysema

M/E:A) Centrilobular emphysema

Dilated respiratory bronchioles (R.B.) with normalA.D. and alveoli.

B) Panacinar emphysema.

l) Alveoli are:

Few in number, increased in size, distorted inshape.


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Emphysema

2) Interalveolar septa: Thin and in advanced stages, alveolar septa

rupture.

The interalveolar capillaries are compressed bydilated air spaces.


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http://www.microscopyu.com/galleries/pathology/emphysemalarge.htmlhttp://www.microscopyu.com/galleries/pathology/emphysema.html


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Emphysema

Complications:l) Respiratory system:Ch. bronchitis.Interstitial emphysema.Spontaneous pneumothoraxRespiratory failure.

2) C. V. S.:pulmonary hypertension and right sided heart

failure.


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Other types of Emphysema

I- Obstructive Hyperinflation (emphysema)

II- Compensatory Hyperinflation(Emphysema)

III- Senile (Atrophic) hyperintlation(emphysema)

IV- Interstitial Emphysema:


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Pneumonitis

Inflammation of lung tissue.

Classification1) Bacteria1:

- Lobar pneumonia.

- Bronchopneumonia.2) Primary Atypical Peneumonitis

3) Loeffler's Pnueumonia

4) Granuloma

5) Lipid Pneumonia6) Irradiation Pneumonia


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Lobar Pneumonia

Acute bacterial infection involving at least an entire lobe oflung (due to streptococcus pneumonia in 95 % of cases)

Incidence:

It predominates in middle-aged males.

Method of infection:By inhalation. (droplet infection)


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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

interalveolar pores to involve the whole lobe andthe pleura.

Lobar PneumoniaLobar Pneumonia


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5- The fluid together with the cellular exudate expelair away from the alveoli producing a firm airlesslobe leading to consolidation (hepatisation) of the

affected lobe.

Pathology:Sero-fibrinous inflammation of lung that passes in

the following stages.



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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 andscattered neutrophils.



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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).



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M/E:1- Inter-alveolar cappillaries still congested.

2- The alveoli are filled with exudate formed of fibrin

network entangling in its meshes excessneutrophils, R.B.Cs., few macrophages withbacteria.



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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.



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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



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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 isreabsorbed through lymphatics or blood vessels orremoved by macrophages and rarely coughed up.



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N/E:1- The affected lobe:

- The size decrease gradually until it becomes normal withrestoration of the normal color.

- The consistency becomes as wet sponge and is finallyairful.

2- Cut surface: Wet, smooth and exudes a frothy creamyfluid.

3- Pleurisy resolves.

4- Hilar lymphadenitis disappears.



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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.



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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).

Complications of Lobar PneumoniaComplications of Lobar Pneumonia


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Bacterial BronchopneumoniaBacterial Bronchopneumonia

Acute bacterial infection of the bronchioles and thesurrounding alveoli.

Aetiology:

1) Staphylococcus aureus.2) Streptococcus pyogens.

3) Pnoumococous.

4) haemophilus influenza

Mode of infection: by inhalation.


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Types:1) Primary bronchopneumonia: Due to 1ry (exogenous) invaders.

Extremes of age.2) Secondary bronchopneumonia:

Due to 2ry (endogenous) invaders whichcomplicate other diseases.


B t i l B h iB t i l B h i


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PathologyAcute suppurative inflammation of bronchioles andsurrounding 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.



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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.



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M/E: Patchy affection of bronchioles and

surrounding alveoli of acute suppurativebronchiolitis at different stages ofdevelopment. . The surrounding alveoli are filled with

pus rich in inflammatory cells and pus

cells. Interalveolar septa are acutely inflamed.



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Complications:Complications:1. In lung:

Lung abscess and gangrene.

Lung fibrosis, leading to pulmonary hypertension andright-sided head failure.

Bonchiectasis.

2. In pleura:

Empyema.



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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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Pathology of COPD 2009