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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)1(Chronic Bronchitis
2) Subepithelial Tissue:chronic inflammatory cell
infiltrations.
Bronchial mucous glands arehyperplastic, hyperactive withprogressive fibrosis.
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)1(Chronic Bronchitis
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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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
inter- alveolar 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.
Lobar PneumoniaLobar Pneumonia
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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.
Lobar PneumoniaLobar Pneumonia
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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).
Lobar PneumoniaLobar Pneumonia
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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.
Lobar PneumoniaLobar Pneumonia
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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.
Lobar PneumoniaLobar Pneumonia
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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
Lobar PneumoniaLobar Pneumonia
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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.
Lobar PneumoniaLobar Pneumonia
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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.
Lobar PneumoniaLobar Pneumonia
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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.
Lobar PneumoniaLobar Pneumonia
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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.
Bacterial BronchopneumoniaBacterial Bronchopneumonia
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.
Bacterial BronchopneumoniaBacterial Bronchopneumonia
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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.
Bacterial BronchopneumoniaBacterial Bronchopneumonia
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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.
Bacterial BronchopneumoniaBacterial Bronchopneumonia
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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.
Bacterial BronchopneumoniaBacterial Bronchopneumonia
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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.
Bacterial BronchopneumoniaBacterial Bronchopneumonia
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Thankyo
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