Emphysema Flashcards
Emphysema
Permanent dilation of airways distal to terminal bronchioles, abnormal dilation of alveoli destruction of alveolar walls.
Aetiology
Smoking
Pollution
Genetics
Inflammation and WBC activity leads to tissue damage
Free radicals, proteases, elastase, collagenous
Neutrophils and macrophages release proteases that destroy lung tissue. But in lobar pneumonia there are masses of neutrophils but little alveolar damage.
Lung tissue is usually protected by antiproteases and antioxidants
Eg. When exposed to spoke, elastase may be introduced which causes damage to tissues- neutrophil elastase
Antiproteases
Protect tissue by inhibiting protease (neutrophil elastase) activity
Balance of antiproteases and proteases
If proteases increase, more damage to lung tissue causing emphysema. (Smoking, pollution)
Smoking causes an increase in release of proteases from WBCs. Causes increase in WBCs.
If antiproteases decrease, there’s less protection from proteases, causing emphysema (genetics, smoking, liver injury).
Genetics- alpha-antitrypsin deficiency. Produced but remains in liver cell, leading to lung and liver disease. Some people born with low levels naturally. Decreased from liver disease. Smoking- antiproteases inefficient in inhibiting the elastase
Complications
Dyspnea- loss of elastic recoil, retention of dead air. Loss of surface area, particularly in alveoli
Obstruction on emphysema caused by loss of elastic recoil, thus reducing pressure
Progressive dyspnea- hyper inflated lungs
Comorbidity of COPD
Cardiovascular disease eg ischaemic heart disease, stroke, pulmonary embolism - may be due to same risk factors
Cancer- similar risk factors
Osteoporosis - smoking, inflammatory mediators, glucocorticoids
Emphysema
Permanent dilation of airways distal to terminal bronchioles, abnormal dilation of alveoli destruction of alveolar walls.
Aetiology
Smoking
Pollution
Genetics
Inflammation and WBC activity leads to tissue damage
Free radicals, proteases, elastase, collagenous
Neutrophils and macrophages release proteases that destroy lung tissue. But in lobar pneumonia there are masses of neutrophils but little alveolar damage.
Lung tissue is usually protected by antiproteases and antioxidants
Eg. When exposed to spoke, elastase may be introduced which causes damage to tissues- neutrophil elastase
Antiproteases
Protect tissue by inhibiting protease (neutrophil elastase) activity
Balance of antiproteases and proteases
If proteases increase, more damage to lung tissue causing emphysema. (Smoking, pollution)
Smoking causes an increase in release of proteases from WBCs. Causes increase in WBCs.
If antiproteases decrease, there’s less protection from proteases, causing emphysema (genetics, smoking, liver injury).
Genetics- alpha-antitrypsin deficiency. Produced but remains in liver cell, leading to lung and liver disease. Some people born with low levels naturally. Decreased from liver disease. Smoking- antiproteases inefficient in inhibiting the elastase
Complications
Dyspnea- loss of elastic recoil, retention of dead air. Loss of surface area, particularly in alveoli
Obstruction on emphysema caused by loss of elastic recoil, thus reducing pressure
Progressive dyspnea- hyper inflated lungs
Comorbidity of COPD
Cardiovascular disease eg ischaemic heart disease, stroke, pulmonary embolism - may be due to same risk factors
Cancer- similar risk factors
Osteoporosis - smoking, inflammatory mediators, glucocorticoids
Systemic effects of COPD
Weight loss, especially if skeletal muscle mass, increased work of breathing, frequent respiratory infections require more energy
