Pathophysiology of COPD Flashcards
What is COPD?
-persistent airflow limitation usually progressive and associated with an enhanced chronic inflammatory response in the airways and lungs to noxious particles or gases
What is the predominant cause of COPD?
smoking
What are the characteristics of the obstructed airflow in COPD sufferers?
- not fully reversible
- doesn’t change over months
- progressive in the long term
Two factors that contribute to the severity of COPD in patients?
Exacerbations and Comorbidities
When do exacerbations occur?
when symptoms worsen rapidly beyond normal day-to-day variations requiring a change in treatment.
Symptoms of COPD?
- chronic and progressive dyspnoea
- chronic cough
- chronic sputum production
Risk factors of COPD?
- genes
2. exposure to particles i.e. tobacco, dust, heating and cooking air pollution, outdoor air pollution
Two classes of COPD?
- chronic bronchitis
2. emphysema
what is chronic bronchitis?
- a chronic cough with sputum production lasting at least 3 months
- the bronchioles lose shape and are blocked with mucus.
what is emphysema?
- a chronic cough caused by shortness of breath
- alveolar walls destroyed forming larger but fewer alveoli
what happens when an individual is exposed to COPD risk factors?
- neutrophils and macrophages accumulate in alveoli
- they become activated and release granules containing elastase and matrix metalloproteinases (MMP)
- resulting in damage and elastic tissue destruction
- hence inflammation
What is the protease/antiprotease imbalance theory?
- this is when there is a deficiency in congenital or functional alpha1 anti-trypsin
- hence causing an unbalance b/w the destructive protease activity and the protective antiprotease activity
define congenital and functional?
congenital - a trait since birth
functional - a trait developed as a result of an event
what is the consequence of tissue damage in the lung?
airway obstruction (dyspnoea)
Explain how tissue damage in the lungs causes dyspnoea in relation to elastic tissue?
- inflammatory infiltration of walls with neutrophils, macrophages, B cells and T cells
- loss of elastic tissue
- respiratory bronchioles collapse during expiration
- dyspnoea
Explain how tissue damage in the lungs causes dyspnoea in relation to thickening of bronchiole walls?
- Inflammatory infiltration of the walls with neutrophils, macrophages, B cells and T cells.
- Smooth muscle hypertrophy and fibrosis
- Bronchiole wall thickens
- Dyspnoea
Explain how tissue damage in the lungs causes dyspnoea in relation to goblet cells?
- inflammatory infiltration of the walls with neutrophils, macrophages, B cells, T cells
- Goblet cell metaplasia with mucus accumulating in the lumen
- Dyspnoea
What are the common causes of exacerbations?
- Viral upper respiratory tract infections
2. Infection of tracheobronchial tree
What are the clinical presentations of COPD exacerbations?
- Dyspnoea
- Chest pain
- Cough
- Fever
- Altered mental status
What are the comorbidities of COPD?
- Cardiovascular disease
- Osteoporosis
- Respiratory infections
- Anxiety and depression
- Diabetes
- Lung cancer
- Serious infections
- Bronchiectasis
How is COPD diagnosed?
- Using spirometry
- chest radiograph
- full blood count to check for anaemia and polycythaemia
- BMI calculated
What does a post-bronchodilator FEV/FVC value if less than 0.70 mean?
Shows presence of airflow limitations
Compare results to normal value for that age
How can you differentiate between COPD an Asthma?
- If FEV AND FEV/FVC values return to normal after drug therapy
- If there’s a large response to bronchodilator or 30mg prednisolone after 2 weeks treatment
- Serial peak flow measurements show day-to-day variability
(All these show signs of asthma and not COPD)
What are therapeutic options for treating COPD?
- Smoking cessation (pharmacotherapy and NRT)
- Encourage regular physical activity
- Flu and pneumonia vaccines should be given
Do any of the available treatments of COPD modify the long te decline in lung function?
Nope
What are the two classes of bronchodilators?
Short-acting and long-acting
What are short acting bronchodilators used to treat COPD?
They are bronchodilators that ease COPD symptoms that come and go.
What are long acting bronchodilators used to treat COPD?
They are bronchodilators used to prevent breathing problems in those whose symptoms don’t go away.
What are examples of short-acting bronchodilators?
- Anticholinergics (ipratropium)
- Beta2-agonists (albuterol)
- A combination of the two (ipratropium and albuterol)
What are examples of long acting bronchodilators?
- Anticholinergics (tiotropium)
- Beta2-agonists (formeterol)
- Combination of the two
- Combination of beta2-agonist with a corticosteroid medicine
Ipratropium is a muscarinic (m2) antagonist. How does this work as an anticholinergic?
Inhibits acetylcholine binding to muscarinic receptors on bronchial smooth muscle hence preventing signal transduction!
What do anticholinergics do?
Dilate the airways preventing bronchospasm and reducing mucus production
How do beta2-agonists work?
- They bind to the beta2-adrenergic receptor
- Adenylyl Cyclase is activated via Gs protein hence increasing cAMP levels and activating protein kinase A (PKA)
- PKA phosphorylates proteins that mediate bronchial smooth muscle relaxation causing them to relax
