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WEEK 18:
Lung pathology- obstructive lung disease (COPD + Bronchiectasis):
| Question | Answer |
|---|---|
| balance between what helps protect lungs (2) | protease (elastase) and anti proteases (a1 anti-trypsin) |
| why is a balance between protease and anti-protease enzymes needed | inflammatory cells (macrophages + neutrophils) in lungs release proteases which break down proteins so lung is protected with anti-proteases |
| anti-protease production is affected by (2) | inherited deficiency in a1 anti-trypsin and smoking (stimulates activation of elastases and proteases) |
| what does affected anti-protease production lead to (2) | uncontrolled proteolysis and destruction of elastic tissue |
| describe the oxidant antioxidant imbalance in lungs leading to proteolysis | normal lung has anti-oxidants but smoke has ROS (free radicals) causing tissue damage which stimulates inflammatory cells leading to production of antiproteases |
| obstructive disease (6) | COPD, bronchitis, emphysema, asthma, bronchiectasis, and cystic fibrosis |
| overview of COPD | chronic and irreversible limitation of airflow in and out of respiratory tree, made of chronic bronchitis and emphysema , due to smoking/ urban pollution |
| clinical definition of chronic bronchitis | persistent productive cough for at least 3 consecutive months in at least 2 consecutive years with mucus hypersecretion and present inflammatory cells |
| emphysema | irreversible dilation of respiratory bronchioles + alveoli leading to destruction of elastic tissue, increased mucous secretion, and coalescence of sacs, affecting gas exchange and causing obstruction |
| types of emphysema (anatomical location) | centriacinar (CA)/ centrilobular and pan acinar (PA)/ pan lobular |
| centriacinar (CA)/ centrilobar emphysema | most common and more common in upper lobes where respiratory bronchioles are dilated due to smoking |
| pan acinar (PA)/ pan lobular emphysema | hereditary condition causing dilated alveoli which is more common in lower lobes |
| AATD in emphysema | inherited condition of AATD (a1 anti trypsin deficiency- protease inhibitor) can lead to emphysema |
| emphysema presentation (7) | SOB, prolonged expiration, barrel chest due to use of accessory muscles, prolonged onset >40 years, later presentation of AATD, often with chronic bronchitis (cough + mucus), and pursed lips |
| features of CT scan/ histology of emphysema | big hole in emphysema = decrease SA* |
| how does chronic bronchitis narrow the airway | changes in the airway (enlarged mucus secreting glands, more goblet cells, oedematous mucosa and fibrosis of bronchiolar wall) leads to narrowing |
| bronchiectasis | permanent dilation of main bronchi and bronchioles whilst surrounding scar tissue contracts (occurring after pulmonary inflammation and scarring) |
| symptoms of bronchiectasis | chronic cough with dyspnoea, production of large amounts of foul-smelling sputum, haemoptysis from damaged epithelium, and clubbing |
| infection as the pathogenesis of bronchiectasis | persistent and recurrent infection weakens bronchial walls |
| obstruction as the pathogenesis of bronchiectasis | interference with drainage of bronchial secretions due to tumours or foreign bodies |
| congenital/ hereditary as the pathogenesis of bronchiectasis (3) | CF (a lot of viscoid mucus), immunodeficiency of immunoglobulins lead to infection, and Kartagener syndrome (impaired mucocillary clearance) |
| morphology of bronchiectasis | in both lower lobes, bronchi + bronchioles become more vertical and expanded (4x) |
Created by:
kablooey
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