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DIFFUSION
VENTILATION HYPOXEMIA
HYPERVENTILATION
PERFUSION
HYPO-
CAPNIA
• Restrictive (parenchyma)
– Reduced expansion - < lung volume,<FVC< TLCO, N-EFR
– FEV1:FVC normal; PEFR- normal
– Increased lung density on CXR
– Chest wall disorders (GB syndrome, Polio)
– Interstitial disease
• Acute: ARDS, pneumonia
• chronic (pneumoconiosis and infiltrative condition)
Characteristic of COPD
• Group of condition with chronic or recurrent
obstruction to airflow resulting in dyspnea
• Major cause of morbidity
– Cigarette smoking
– Environmental pollutants
COPD
• 1. Emphysema
• 2. Chronic bronchitis
• 3. Bronchiectasis
• 4. Bronchiolitis
• 5. Bronchial asthma
Characteristic of COPDS
• 1. Emphysema
– Acinus - Beyond terminal bronchiole
– Permanent (irreversible) Airspace enlargement
– Wall destruction
– Dyspnea
• TOBACCO AND A1AT DEFICIENCY (ZZ GENOTYPE)
Emphysema
• Permanent enlargement of airways
• Distal to terminal bronchiole
• Destruction of wall
• Without fibrosis
Pathogenesis of emphysema
• Protease- antiprotease imbalance
• Oxidant – antioxidant imbalance
» TOBACCO
» AIR POLLUTION
Types of chronic bronchitis
• Chronic cough, sputum for 3months/yr for 2 yrs
• Infection
• Obstruction- atelectasis (collapse)
• Bronchial hyperresponsiveness.
Pathogenesis of Atopic asthma?
• Childhood onset- triggered by
– Environmental triggers- dusts, dandar, foods
– Positive Family history of atopy.
– Asthma preceded by Urticaria, eczema, allergic
rhinitis
– Classical Type I IgE mediated HSR by mast cells
and eosinophils.
Phases of Asthma
• Acute/ immediate phase response
– Presensitized IgE coated mast cells exposed to same antigen
– Occur within minutes after stimulation.
– Directly or via neuronal reflexes- the mediators- bronchoconstriction,
vaso-permeability, mucus secretion, hypotension, eosinophils influx.