COPD- CHRONIC OBSTRUCTIVE PULMONARY DISEASE

DR. T.Matumithra MD DNB(Pathology)Assistant Professor

OBSTRUCTIVE AND RESTRICTIVE LUNG DISAEASES OBSTRUCTIVE DISEASE:restriction to airflow entry(eg: mucous

plugs, bronchoconstriction) RESTRICTIVE LUNG DISEASE:Restriction to expansion of

alveoli( interstial lung disease, pneumoconioses)

OBSTRUCTIVE LUNG DISEASE 1. Emphysema 2. Chronic bronchitis 3. Bronchiectasis 4. Asthma

COPD

1. EMPHYSEMAabnormal permanent enlargement of the

airspaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis.

Types of emphysemaAccording to its anatomic distribution within

the lobule, a. Centriacinar (centilobular)b. Panacinar (panlobular)c. Paraseptal (distal acinar)d. Irregular First two cause clinically significant airflow

obstruction Centriacinar type constitute >95% of cases

a. Centriacinar Emphysema The central or proximal part of the acini -

affected. both emphysematous & normal airspaces exist

in a acinus More frequent in heavy smokers

Centriacinar Emphysema

b. Panacinar Emphysema

The acini are uniformly enlarged

Lower lung lobes

associated with α1-antitrypsin (α1-AT) deficiency

Panacinar Emphysema

c. Distal Acinar Emphysema(Paraseptal Emphysema)

The proximal portion of the acinus is normal, but the distal part is predominantly involved

More severe in the upper half of lungs Characteristic findings are multiple,

continuous, enlarged airspaces from 0.5 cm to >2cm in dia

Irregular Emphysema

The acinus is irregularly involved, and is almost invariably associated with scarring (airspace enlargement with fibrosis)

In most instances foci of irregular emphysema are asymptomatic & clinically insignificant

Bullous Emphysema

Defined as subpleural emphysematous spaces >1-2 cm in diameter

Rupture of bullae may result in pneumothorax

Bullous Emphysema

Pathogenesis of emphysema: Protease – antiprotease theory

Alpha 1 antitrypsin

Elastase(PMN, macrophage)

Elastic damage Emphysema

Smoking

Smoking & emphysema Smokers have greater numbers of

neutrophils & macrophages in their alveoli

Smoking stimulate release of elastase(protease) from neutrophils

Oxidants in smoke & free radicals released by neutrophils inhibit alpha 1 antitrypsin (functional alpha 1 antitrypsin deficiency)

Alpha 1 antitrypsin deficiency

Geno Type % of Population

Normal Pi MM 95% - 97%

Heterozygote Pi MZ 3% - 5%

Homozygote Pi ZZ 0.07% - 0.2%

More than 80% of PiZZ phenotype develop symptomatic emphysema

Clinical course Do not manifest until at least 1/3rd of

functioning lung parenchyma is damaged Dyspnea- insiious , slow progressive Cough and expectoration(ass with chronic

bronchitis) Weight loss barrel chested , sits forward in hunched up

position, breaths through pursed li\psExpiratory airflow limitation, measured

through spirometry, is the key to diagnosis

Mysterious boiling river

2.Chronic Bronchitis Is defined clinically as persistent cough

with sputum production for at least 3 months in at least 2 consecutive years

Tends to affect middle-aged men who are smokers.

Types of chronic bronchitis A. Simple chronic bronchitis

Have productive cough but no evidence of airway obstruction

B. Chronic asthmatic bronchitis Hyperreactive airways with intermittent

bronchospasm & wheezing

C. Obstructive chronic bronchitis Chronic airflow obstruction with emphysema

(in chronic smokers)

Chronic Bronchitis-Pathogenesis

Chronic irritation by inhaled substances (cigarette smoking is the single most important factor)also grains, cotton & silica dust.

4 – 10 times more common in smokers..

Pathogenesis (cont) Tobacco irritants elicit inflammatory

mediators hypertrophy of the submucosal glands in the

trachea and bronchi hypersecretion of mucus in the large airways

smoking impairs ciliary apparatus- predisposes to infection

Morphologic Correlates Of Chronic Bronchitis1. Edematous mucous membrane with

Mucous hypersecretion and plugging 2. Goblet cell metaplasia3. Hypertrophy and hyperplasia of

mucosal glands (Reid Index – normal .4)- increased reid index

4. Lymphocytic infiltration

Clinical features

1.Persistent cough with sputum production. 2.Dyspnea on exertion. 3.hypercapnia, hypoxemia, and mild

cyanosis.

Death may also result from further impairment of respiratory function incident to acute intercurrent bacterial infections.

Clinical course in Emphysema & Chronic Bronchitis

Predominate Bronchitis

Predominant Emphysema

Age (Yr) 40-45 50-75Dyspnea Mild; late Severe; earlyCough Early; copious

sputumLate; scanty sputum

Infections Common OccasionalCor pulmonale

Common Rare; terminal

THANK U

THANK U

Bronchiectasis

Bronchiectasis is characterized by permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue, resulting from or associated with chronic necrotizing infections.

Bronchiectasis Obstructive

Tumor Foreign body Concretions/secretions

Non-obstructive Post-infective Inherited disorders – cystic fibrosis,

immunodeficiency, and immotile cilia syndrome

Kartagener Syndrome

Defect in ciliary motility due to structuralabnormality in the cilia (absence of dyneinarms) Situs invertus Bronchiectasis Sinusitis

Bronchiectasis

Lung shows markedly dilated bronchi andbronchioles, that can be traced up to pleural surfaces.

Bronchiectasis - clinical Features Chronic productive cough Hemoptysis Dyspnea and wheezing Pneumonia, abscess Systemic: fever, weight loss, weaknessLess frequent complications: Cor pulmonale Metastatic brain abscesses & Amyloidosis

Condition(OPD)

Site PathologicChanges Cause Signs

Chronic bronchitis

Bronchus

Mucous gland hyperplasia, hypersecretion

Smoking, pollution

Cough & sputum

Bronchi-ectasis

Bronchus

Airway dilation & scarring

Persistent or severe infection

Cough, fever, sputum

Asthma Bronchus

Smooth muscle hyperplasia, excess mucus, inflammation

Immunologic or unknown

Wheezing cough dyspnea

Emphy-sema Acinus

Airspace enlargement; wall destruction

Tobacco smoke Dyspnea

Small airway disease

Bronch-iole

Inflammatory scarring/oblite-ration

Smoking, pollution

Cough, dyspnea