COPD: Clincal presentation&pathophysiology Flashcards
What causes COPD?
- ) Tobacco smoking (active& passive)
- )Biomass fuel exposure
- ) Occupational exposures (organic&inorganic dusts, chemical agents, fumes)
Oxidative stress may result in the pathological changes of COPD; what can prevent this oxidative stress?
- Antioxidants
- Antiproteases
How can inflammation present in COPD
- Increased neutrophils, macrophages and T cells (CD8>CD4) in the lungs
- Extent of the inflammation related to the degree of airflow obstruction
- Inflammatory pattern is markedly different from asthma-eosinophilic inflammation
Describe some inflammatory mediators involved in inflammation
- Leucotriene B4- neutrophil and T cell chemoattractant
- Chemotactic factors e.g IL-8 and growth related oncogene alpha. Amplify pro-inflammatory responses
- Pro-inflammatory cytokines e.g TNF-alpha, IL-1Beta and IL-6
- Growth factors e.g TGF-Beta, cause fibrosis in the airways
What are the sources of oxidative stress contributing to COPD
- cigarette smoke
- reactive oxygen&nitrogen species from inflammatory cells
What is the role of oxidative stress in COPD
- Markers of oxidative stress are increased in stable COPD (further increased in exacerbations)
- Oxidative stress: inactivates antiproteases; stimulates mucus production; amplifies inflammation by enhancing transcription factor activation (e.g NF kB) and gene expression of pro-inflammatory mediators
Describe the pathophyisology of the airway involved in COPD in terms of mucus hypersecretion
- There’s hypertrophy and hyperplasia of bronchial submucosal glands
- increased number of goblet cells in bonchioles
- destruction of cilia, therefore there’s a difficult expectorating as the sputum gets stuck
Describe the pathophyisology of the airway involved in COPD in terms of the airways
- Narrowing of airways: due to remodeling, starting with smaller airways <2mm
- Increased airways resistance
Why are the smaller airways more susceptible to narrowing?
They don’t have cartilage keeping them open.
Describe the pathophyisology of the airway involved in COPD in terms of the lung parenchyma
- Proteolytic enzymes destroy alveolar tissue
- Elastin &collagen are destroyed (reduced elasticity and structural integrity of the lungs, leading to a loss of elastic recoil.
Airflow obstruction, loss of lung elasticity, loss of alveoli and airway inflammation are all associated with COPD. What presentations of the disease do these bring?
- Expiratory flow limitation
- decreased elastic recoil of lungs
- decreased gas exchange
- Hyperinflation
- Sputum production
What clinical features does COPD give?
- Dyspnoea
- Exercise limitation
- Wheeze
- Sputum
- Increased RR
- Accessory muscle use
- Reduced chest expansion
- Barrel chest
- Reduced breath sounds
- Asterixis
- Cyanosis
- Cor pulmonale
What are the extrapulmonary features of COPD?
- Weight loss
- Muscle wasting
- Cardiovascular comorbidities
- Depression
- Osteoporosis
What do we use to diagnose COPD?
- symptoms
- spirometry (needs to be obstructive)
How do we assess the severity of COPD?
- %FEV1 predicted
- symptoms
Outline the significance of compliance in various respiratory diseases.
- Stiff lungs have low compliance( high elastic resistance)
- Lung fibrosis (scarred/stiff)=low compliance, increased lung recoil, reduced FRC
- Emphysema (tissue destruction/floppy)= high compliance, floppy lungs, reduced lung recoil, increased FRC(barrel chest)
- Asthma doesn’t usually affect compliance
What is FRC
- Functional residual capacity
- The volume of air present in the lungs at the end of passive expiration.
- At FRC, the opposing elastic recoil forces of the lungs & chest wall are in equilibrium and there’s no exertion by the diaphragm or other respiratory muscles.
What is the likely state of the lungs of a patient with COPD?
- Hyperinflated
- FRC& RV are increased
- so gas trapping occurs in expiration
What is the consequence of an expiratory flow limitation (EFL) in tidal breathing?
- RR increases during exercise
- FRC increases despite expiratory muscle activity
- Inspiratory capacity and inspiratory reserve volume decreases
Outline 3 differences between a healthy lung and a lung of a COPD patient.
- Reduced recoil
- Reduced tethering
- Increased airways resistance
Describe the limitation of expiratory flow in a COPD patient
- Expiratory flow limitation occurs when flow doesnt increase with increasing expiratory effort
- In COPD this can occur during tidal breathing
- Since maximum expiratory flow is reached during tidal breathing, the minimum time for lung emptying is fixed (so you can’t empty lungs faster by pushing harder in expiration)
- This results in a trapped volume
What is dynamic hyperinflation (DH)?
a phenomenon that occurs when a new breath begins before the lung has reached the static equilibrium volume.
What are the consequences of DH?
- Forces COPD patients to breathe at higher lung volumes
- Lower lung compliance
- Higher work of breathing
- Limitation of tidal volume expansion
Describe the neural respiratory drive of a person with COPD
- There’s an increased respiratory load
- There’s a reduced muscle pump capacity(due to hyper inflammation and functional diaphragm weakness)
How may someone with COPD present?
- Increased RR
- Accessory muscle use
- Wheeze
- Reduced chest expansion
- Barrel chest
- Reduced breath sounds
- Asterixis
- Cyanosis
- Cor pulmonale
How may pulmonary hypertension develop in someone with COPD?
- Chronic hypoxia leads to pulmonary vasoconstriction which leads to pulmonary hypertension
- Muscularisation, intimal hyperplasia,fibrosis and obliteration may also cause pulmonary hypertension
What may be the consequence of pulmonary hypertension
- May cause cor pulmonale, leading to death
- May also result in oedema
- oedema may also be caused by renal and hormonal changes
What is the function of the bronchial mucinous glands?
- Responsible for the production of most of the mucus
- Present in the main bronchi
What happens to the bronchial mucinous glands (in the main bronchi) in COPD
- smoke causes exposure to irritants & chemicals
- These irritants and chemicals cause hypertrophy &hyperplasia of the bronchial mucinous glands
What is the function of the goblet cells
- mucous production
- Present in the smaller airways
What happens to the FEV1/FVC ratio of a COPD pt
- FEV1 decreases significantly more than FVC decreases
- Result is a much lower FEV1/FVC ratio
- The normal FEV1/FVC ratio is~ 70-80% in normal adults; a value <70% indicates airflow limitation & possible COPD
What is the role of age in COPD
-COPD is favoured by age of onset>35yrs
How is chronic bronchitis defined
chronic cough, sputum production on most days for 3 months of 2 successive yrs
Explain the distinction between the terms ‘blue bloaters’ and ‘pink puffers’
- ) BLUE BLOATERS= mostly chronic bronchitis
- have a decreased alveolar ventilation
- low pao2 and high paco2
- cyanosed
- not breathless
- may develop cor pulmonale
- Their resp. centres are very insensitive to co2
- supplementary oxygen should be given with care cos they rely on their hypoxic drive - )PINK PUFFERS=mostly emphysema
- near normal pao2
- normal/low paco2
- increased alveolar ventilation
- not cyanosed
- breathless
- may progress to type 1 respiratory failure
