Obstructive Pulmonary
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Transcript of Obstructive Pulmonary
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COPD
SS Visser, PulmonologyInternal Medicine
UP
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Chronic Obstructive pulmonary
Disease
Two distinct processes are involved, most often in
combination. Chronic Bronchitis dx on history
Emphysema dx previously on histology,
nowadays clinically (good clinical-pathologic-
radiologic correlation)
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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
hyperreactivity.
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Def: Emphysema
Permanent abnormal distention of air spaces distal to the
terminal bronchiole with destruction of alveolar septa
(containing alveolar capillaries) and attachments to thebronchial walls.
Classification:
1. Centriacinar ( centrilobular) emphysema
2. Panacinar emphysema
3. Paraseptal emphysema
4. Senile emphysema
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Def: COPD
Chronic obstruction to airflow due to chronic
bronchitis 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
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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
oprevalence in low birth weight and lowsocioeconomic status
Tuberculosis in smokers predisposes to COPD
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Pathogenesis:Effects of
Smoking -1
Oxidative stress: O2-, OH-,H2O2, HOCl; source of Fe
2+pcatalizes production of OH-by neutrophils, eosinophils,
alveolar macrophages; tar (cigarettes) contains NO andinduces iNOSptoxic peroxynitrites
Elastin breakdown- activated neutrophilspneutrophilelastases and oxidants; E-1-AT and metalloproteinaseinhibitors (lung defenses) inactivated by smoke
Chemoattractant, upregulation of adhesion moleculespneutrophil sequestration in lungs
oexpression of pro-inflammatory mediators: IL-8, NF-OBprecruitment of N, B, E and T lymphocytes
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Effects of smoking -2
o levels of myeloperoxidase and eosinophilic cationic
proteinpbronchoconstriction o levels of TGF-F (transforming growth factor)pfibrogenesis
Lipid peroxidation and DNA damageppoint mutations 0f
the p53 gene locusp
epithelial dysplasia and lungcancer q ciliary functionp retained secretions; o airway resistancepvagal-mediated smooth muscle contraction
Hypertrophy and hyperplasia of mucus secreting glands
posecretions
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Pathogenesis-3
Air pollutionpexacerbations of CB related to heavypollution with SO2 and NO2
Occupation p exposure to organic and inorganic dust ornoxious gasespaccelerated decline in lung function
Infectionp even mild viral respiratory infections ( rhinovirus) may be a major factor associated with etiology aswell as progression of disease; severe viral pneumonia early
in life may lead to COPD
Genetic factors: - E-1-antitrypsin deficiency PIZZ, PISZ,PI00 (PI null null), o susceptibility to effects of smoking
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Pathophysiology
Air trapping- RV and FRC elevated
Hyperinflation TLC elevated
q elastic recoil pressurep dynamic collapse of airways
during expirationpineffective cough mechanism andpursed lips breathing (emphysema)
o compliance (emphysema) o airway resistance
Prolonged forced expiratory time (N=
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Pathology: CB
Hypertrophy of mucus-producing glands in submucosa of
large cartilaginous airways
Goblet cell hyperplasia, mucosal and submucosal
inflammatory cell infiltrate, oedema, peribronchial fibrosis,
intraluminal mucus plugs and increased smooth muscle in
small airways
The major site of airflow obstruction is in the small airwaysand the inflammatory infiltrate consists of neutrophils (in
asthma eosinophils)
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Pathology : Emphysema
oin number and size of alveolar fenestraepeventualdestruction of alveolar septa and their attachments to
terminal and respiratory bronchiolespdistention ofalveolar spaces
1. Centriacinar E- respiratory bronchioles (central) affected
2. Panacinar E- central and peripheral portions of acinusaffected
3. Senile E- alveoli and alveolar ducts enlarge (> 50 Y)
4. Periacinar/paraseptal E- distention of alveolar spacesadjacent to septal and pleural surfaces
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Emphysema:ChronicBronchitis
Emphysema = pink puffer
Age (Dx) 60 + y
Rest dyspnea mild-mod
Exer dyspnea severe
Cough
Sputum scanty, mucoidResp infect less often
Resp failure terminal
Cor pulmonale terminal
Chronic Bronchitis = blue
bloater
50 y
none
moderate
prominent
large volume, purulentoften
repeatedly
common
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Emphysema:Chronic BronchitisPHT (rest) 0-mild
(exertion) moderate
Build Asthenic, cachecticHematocrit 35-45
Breath pattern useaccessory muscles ofrespiration
Sleep pattern Normal
XRC Hyperinflation
Bullae
Mild-moderate
severe
obese, cyanosed
50-55
do not use accessory muscles
of respiration
sleep apnea
o bronchovascular markings
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Emphysema:Chronic Bronchitis
Blood gas:
PaO2 65 mm Hg
PaCO2 35-40
Elastic recoil qAW resistance N-o
Diffusion Cap q
FEV1 q qBronchodilator
response Poor
45-60
50-60
Normal
o
N- qq
Better but < 12% and 200ml
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Spirometric classification ofCOPD severity using post-
bronchodilator FeV1
Stage I (Mild): FeV1/FVC
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Treatment: Goals of
management -1
Recognition of disease (early Diagnosis and staging)
Smoking cessation (secondary prevention) nicotine
replacement and Zyban Improvement of breathlessness (Rx of airflow obstruction-
bronchodilator drugs)
1.Methylxanthines
2.Short and long-acting B2adrenergic agonists (o
incidence ofpneumonia with ICS and LABA combinations)
3.Short and long-acting Anticholinergics- BD of choice inCOPD
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Treatment -2
Respiratory infections AB when osputum volume and/orpurulence (exacerbation of COPD); Influenza and
Streptococcus pneumoniae vaccination Bronchopulmonary drainage and postural drainage
(physiotherapy) for patients with CB
Oxygen therapy for patients with hypoxia (PaO2
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Treatment -3
Glucocorticoids only 10% of COPD patients showsubjective benefit and improved lung function (FeV1
increase of 20% or more) on systemic GCs; with COPDexacerbation a course of prednisone 40 mg/d for 2 weeks areusually prescribed
Inhaled GCs may q severity of exacerbations and need forhospitalisation. Benefit of 10-14 day trial of 30-40mg
prednisone for Stage III COPD patients remains to beproven.
Lung volume reduction surgery
Transplantation
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Airway Diseases - COPD
Smoking
Hyperinflation Airway collapse
Respiratory infection
Bronchospasm Allergy
Inflammation
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Airway Diseases : Asthma
Allergy
Inflammation Bronchospasm
Hyperinflation
Respiratory infection
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AirwayDiseases:Bronchiectasis
Respiratory infection
Hyperinflation
Bronchospasm
Inflammation
Allergy