Aetiology and prediction: the difference between pathogenesis and prevention
aetiology and pathogenesis of chronic obstructive lung disease
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Transcript of aetiology and pathogenesis of chronic obstructive lung disease
Chronic Obstructive Pulmonary Disease
Kanishk Deep SharmaRoll no. 50
Definition
• “A disease state characterised by progressive development of airflow limitation that is not fully reversible. The airflow limitation is usually progressive and usually results from an abnormal response of lungs to noxious particles or gases”
• Airflow obstruction is defined as reduced FEV1/FVC ratio (< 0.7)
RISK FACTORS
1. Exposure to tobacco smoke. – most significant risk factor – Pipe smokers, cigar smokers and marijuana smokers– second-hand smoke– Nicotine stimulates sympathetic system– Decreased ciliary activity & ciliary loss– Decreased oxygen carrying capacity– Cellular hyperplasia
• Production of mucus• Reduction in airway diameter• Increased difficulty in clearing secretions
2. People with asthma who smoke– increases the risk of COPD
3. Occupational exposure to dusts and chemicals– Long-term exposure to chemical fumes, vapors and dusts in the
workplace can irritate and inflame lungs4. Age
– develops slowly over years5. Genetics
– alpha-1-antitrypsin deficiency– certain smokers more susceptible to the disease
6. Infection– Aggravates COPD progression
CHRONIC BRONCHITIS
• presence of cough and sputum production for at least 3 months in each of 2 consecutive years, is not necessarily associated with airflow limitation
• Hyperplasia of mucus-secreting glands in trachea and bronchi• Bronchioles are clogged with mucus and pose a physical
barrier to ventilation• Increase in goblet cells• Disappearance of cilia• Chronic inflammatory changes and narrowing of small airways• Altered function of alveolar macrophages causing infections• Greater resistance to airflow increases work of breathing• Hypoxemia and hypercapnia develop more frequently in
chronic bronchitis than emphysema
EMPHYSEMA
• Abnormal permanent enlargement of the air space distal to the terminal bronchioles accompanied by destruction of bronchioles
• Small bronchioles become obstructed as result of– Mucus– Smooth muscle spasm– Inflammatory process– Collapse of bronchiolar walls – Recurrent infections causing inflammation,
exudates & edema
• Elastin & collagen destroyed• Bronchioles collapse• Trapped air cause hyperinflation & over
distension• Alveolar wall & capillary destruction• Reduced surface area for oxygen diffusion• Compensatory tachypnea
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