Pathology Flashcards
(120 cards)
Obstructive vs restrictive disease
Airway pathology - Obstructive
Lung pathology - Restrictive
Obstructive airway syndromes
Asthma, COPD, emphysema
What is ACOS
Asthma/COPD overlap syndrome, usually in smokers with reversible COPD and eosinophilia who are steroid responsive. Blood eosinophilia > 4%
What is the asthma triad
Reversible airflow obstruction, airway inflammation and airway hyperresponsiveness
How does asthma evolve
Bronchoconstriction - chronic airway inflammation - airway remodelling
Histological remodelling of basement membrane, submucosa and smooth muscles in asthma
Basement membrane - Thickening
Submucosa - Collagen deposit
Smooth muscles - Hypertrophy
Response of airway cells to allergen in asthma
Dendritic cells take up antigen and present it to naive T cells in the lymph nodes. This causes maturation to Th2 and B cell. Th2 cells release IL5 which stimulates eosinophils to secrete leukotrienes and cytokines. B cells secrete IgE. Mast cells have IgE receptors and degranulate releasing histamine causing bronchoconstriction. Basophils also bind to IgE and secrete Leukotriene D4 which increases mucus secretion. Mast cells release IL-4 which further causes B cells to release IgE.
How can airway inflammation be measured
Bronchoscope and bronchial biopsy
What predisposes patient to airway hyperresponsiveness in asthma
Desquamation due to eosinophil influx
What drugs can cause asthma symptoms
NSAIDS and B blockers
What happens to FEV1/FVC ratio in asthma
< 75% as FEV1 drops by FVC remains normal
Components of COPD
Muco-ciliary dysfunction, tissue damage and inflammation
Disease process in COPD
Irritants such as cigarette smoke activate macrophages and airway epithelial cells. This causes release of neutrophil chemotactic factors including IL 8 and leukotriene B4. Macrophage and neutrophils release proteases that break down connective tissue in lung (emphysema) and stimulate muscus hypersecretion. These are normally counteracted by antiproteases however in COPD, there’s an imbalance between proteases and antiprotease.
What does protease-antiprotease imbalance lead to
Alveolar destruction and emphysema
What are indicators of high risk in COPD
Two exacerbations or more within last year (or)
FEV1 < 50% predicted are indicators or high risk
General symptoms in COPD
Non-atopic, smoker, daily productive cough, progressive breathlessness, frequent infective exacerbations, chronic bronchitis - wheezing, emphysema causing reduced breath sounds
Non pharmacological management of COPD
Smoking caessation, immunisation for influenza/pneumococcal, physical activity oxygen
Smoking caessationg techniques
Nicotine replacement therapy, varenicline, bupropion
Main inflammatory cells in asthma vs COPD
Asthma - Eosinophils, COPD - Neutrophils
Asthma vs COPD cough
Asthma - Non-productive cough whereas COPD is productive
Asthma vs COPD diurnal variation
Asthma has diurnal variation whereas COPD doesn’t
Asthma vs COPD gas exchange
Normal gas exchange in asthma where it’s impaired in COPD
Thoracic restriction not due to lung causes
Skeletal - Kyphoscoliosis, ankylosing spondalitis, multiple rib fracture
Muscle weakness, obesity, ascites
Interstital lung disease are also known as
Diffuse parenchymal lung disease (DPLD)