Obstructive Pulmonary

8/8/2019 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



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AirwayDiseases:Bronchiectasis


Hyperinflation

Bronchospasm

Inflammation

Allergy

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Obstructive Pulmonary