COPD

Chronic Obstructive pulmonary Diseas

e

 Two distinct processes are involved, most often in c

ombination.
 Chronic Bronchitis – dx on history
 Emphysema – dx previously on histology, nowaday
s clinically (good clinical-pathologic-radiologic cor
relation)
 Def: Chronic Bronchitis

 Excessive tracheobronchial mucus production sufficient to

cause cough with expectoration for most days of at least 3
months of the year for 2 consecutive years.
 Classification:
1. Simple chronic bronchitis
2. Chronic mucopurulent bronchitis
3. Chronic bronchitis with obstruction
4. Chronic bronchitis with obstruction and airway hyperreact
ivity.
 Def: Emphysema

 Permanent abnormal distention of air spaces distal to the t

erminal bronchiole with destruction of alveolar septa (cont
aining alveolar capillaries) and attachments to the bronchi
al walls.
 Classification:
1. Centriacinar ( centrilobular) emphysema
2. Panacinar emphysema
3. Paraseptal emphysema
4. Senile emphysema
 Def: COPD

 Chronic obstruction to airflow due to chronic bronc

hitis and/or emphysema.
 Degree of obstruction may be less when the patient
is free from respiratory infection and may improve
with bronchodilator drugs
 Significant obstruction is always present
 Epidemiology of COPD

 30% of smokers develop COPD

 20% of adult males have COPD
 15% of COPD patients are severely symptomatic
 4 th leading cause of death (USA)
 Mortality rate still rising
 prevalence in low birth weight and low socioecon
omic status
 Tuberculosis in smokers predisposes to COPD
 Pathogenesis:Effects of Smokin
g -1
 Oxidative stress: O2-, OH-,H2O2, HOCl; source of Fe2+  c
atalizes production of OH- by neutrophils, eosinophils, alveo
lar macrophages; tar (cigarettes) contains NO and induces i
NOStoxic peroxynitrites
 Elastin breakdown- activated neutrophils neutrophil elas
tases and oxidants; -1-AT and metalloproteinase inhibitors
(lung defenses) inactivated by smoke
 Chemoattractant, upregulation of adhesion molecules  n
eutrophil sequestration in lungs
 expression of pro-inflammatory mediators: IL-8, NF-B 
recruitment of N, B, E and T lymphocytes
 Effects of smoking -2

  levels of myeloperoxidase and eosinophilic cationic protei

n  bronchoconstriction
  levels of TGF- (transforming growth factor) fibrog
enesis
 Lipid peroxidation and DNA damage point mutations 0f t
he p53 gene locus epithelial dysplasia and lung
cancer
  ciliary function  retained secretions;  airway resistance
vagal-mediated smooth muscle contraction
 Hypertrophy and hyperplasia of mucus secreting glands 
secretions
 Pathogenesis-3

 Air pollution exacerbations of CB related to heavy polluti

on with SO2 and NO2
 Occupation  exposure to organic and inorganic dust or no
xious gases accelerated decline in lung function
 Infection  even mild viral respiratory infections ( rhino vir
us) may be a major factor associated with etiology as well a
s progression of disease; severe viral pneumonia early in life
may lead to COPD
 Genetic factors: - -1-antitrypsin deficiency PIZZ, PISZ, PI
00 (PI null null),  susceptibility to effects of smoking
 Pathophysiology

 Air trapping- RV and FRC elevated

 Hyperinflation –TLC elevated
  elastic recoil pressure  dynamic collapse of airways dur
ing expiration ineffective cough mechanism and pursed li
ps breathing (emphysema)
  compliance (emphysema)
  airway resistance
 Prolonged forced expiratory time (N=<6 seconds)
 Pathology: CB

 Hypertrophy of mucus-producing glands in submucosa of la

rge cartilaginous airways
 Goblet cell hyperplasia, mucosal and submucosal inflammat
ory cell infiltrate, oedema, peribronchial fibrosis, intralumin
al mucus plugs and increased smooth muscle in small airwa
ys
 The major site of airflow obstruction is in the small airways
and the inflammatory infiltrate consists of neutrophils (in ast
hma eosinophils)
 Pathology : Emphysema

 in number and size of alveolar fenestrae eventual destr

uction of alveolar septa and their attachments to terminal a
nd respiratory bronchioles distention of alveolar spaces
1. Centriacinar E- respiratory bronchioles (central) affected
2. Panacinar E- central and peripheral portions of acinus affe
cted
3. Senile E- alveoli and alveolar ducts enlarge (> 50 Y)
4. Periacinar/paraseptal E- distention of alveolar spaces adja
cent to septal and pleural surfaces
 Physical signs of COPD

 Ronchi- in early disease present on forced expiration, later p

resent in inspiration and expiration
 Prolonged forced expiratory time (> 6 seconds)
 Hyperinflation:  cardiac dullness, liver dullness displaced
downwards,  A-P chest diameter,  heart and breath sound
s, Hoover sign
 Inspiratory crepitations (lung bases)
 Pursed lips breathing ( dynamic airway collapse)
 Use accessory respiratory muscles
 Signs of cor pulmonale and PHT
 Emphysema:ChronicBronchitis

Emphysema = pink puffer Chronic Bronchitis = blue

bloater
Age (Dx) 60 + y 50 ± y
Rest dyspnea mild-mod none
Exer dyspnea severe moderate
Cough ± prominent
Sputum scanty, mucoid large volume, purulent
Resp infect less often often
Resp failure terminal repeatedly
Cor pulmonale terminal common
 Emphysema:Chronic Bronchitis

PHT (rest) 0-mild Mild-moderate

(exertion) moderate severe
Build Asthenic, cachectic obese, cyanosed
Hematocrit 35-45 50-55
Breath pattern use accesso
ry muscles of respiration do not use accessory muscles
of respiration
Sleep pattern Normal
XRC Hyperinflation sleep apnea
Bullae  bronchovascular markings
 Emphysema:Chronic Bronchitis

Blood gas:
PaO2 ± 65 mm Hg 45-60
PaCO2 35-40 50-60
Elastic recoil  Normal
AW resistance N-

Diffusion Cap 
N- 
FEV1 
Bronchodilator 
response Poor Better but < 12% and 200ml
 Spirometric classification of C
OPD severity using post-bronch
odilator FeV1
 Stage I (Mild): FeV1/FVC <0.7; FeV1 80% of pred
icted
 Stage II (Moderate): FeV1/FVC <0.7; FeV1 50- <8
0% of predicted
 Stage III (Severe): FeV1/FVC <0.7; FeV1 30-<50%
 Stage IV (Very severe): FeV1/FVC <0.7; FeV1 <30
% or <50% but chronic respiratory failure is present
. (GOLD 2007)
 Treatment: Goals of manageme
nt -1
 Recognition of disease (early Diagnosis and staging)
 Smoking cessation (secondary prevention) nicotine replacem
ent and Zyban
 Improvement of breathlessness (Rx of airflow obstruction- b
ronchodilator drugs)
1.Methylxanthines
2.Short and long-acting B2adrenergic agonists ( incidence of
pneumonia with ICS and LABA combinations)
3.Short and long-acting Anticholinergics- BD of choice in COP
D
 Treatment -2

 Respiratory infections –AB when sputum volume and/or p

urulence (exacerbation of COPD); Influenza and Streptococ
cus pneumoniae vaccination
 Bronchopulmonary drainage and postural drainage (physioth
erapy) for patients with CB
 Oxygen therapy for patients with hypoxia (PaO2<55 mmHg,
SaO2 <88% ) and erythrocytosis (Hematocrit>55)
 Pulmonary rehabilitation and education ( improving quality
of life)- exercise program and improved nutrition
 Prevention and treatment of complications (cor pulmonale) a
nd limitation of disease progression
 Treatment -3

 Glucocorticoids –only 10% of COPD patients show subjecti

ve benefit and improved lung function (FeV1 increase of 20
% or more) on systemic GCs; with COPD exacerbation a co
urse of prednisone 40 mg/d for 2 weeks are usually prescribe
d
 Inhaled GCs may  severity of exacerbations and need for h
ospitalisation. Benefit of 10-14 day trial of 30-40mg prednis
one for Stage III COPD patients remains to be proven.
 Lung volume reduction surgery
 Transplantation
 Airway Diseases - COPD

 Smoking
 Hyperinflation
 Airway collapse
 Respiratory infection
 Bronchospasm
 Allergy
 Inflammation
 Airway Diseases : Asthma

 Allergy
 Inflammation
 Bronchospasm
 Hyperinflation
 Respiratory infection
 AirwayDiseases:Bronchiectasis

 Respiratory infection
 Hyperinflation
 Bronchospasm
 Inflammation
 Allergy