copd 2 5-2016 madhu
TRANSCRIPT
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