pathophysiology of COPD Flashcards
define COPD
• Group of conditions characterised by airways obstruction that is not completely reversible
• British Thoracic Society Definition:
A slowly progressive disorder characterised by airways obstruction (reduced FEV1 and FEV1/FVC ratio), which does not change markedly over several months.
2 obstructive airway diseases: asthma + COPD
Global initiative for chronic obstructive lung disease (GOLD) definition:
“A common preventable and treatable disease, characterised by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. exacerbations and comorbidities contribute to the overall severity in individual patients”.
mad
how can we predict mild, moderate and severe COPD?
- Mild: FEV1 50-80% predicted
- Moderate: FEV1, 30-50% predicted
- Severe: FEV1 < 30% predicted
FEV1 is the amount of air you can force from your lungs in one second. It’s measured during a spirometry test
- Have to put in age, height and weight (size of lungs etc) before predicting!
If 20-25: lung function will be at its peak but will go downhill after it
give some facts on COPD
• 6th commonest cause of death (will be 3rd by 2020)
• 35,000 deaths in UK/year (3 million worldwide)
- Equivalent to 1 death every 15 mins (4 during this lecture)
• 30,000,000 working days are lost/year
• 95% of cases are smoking related (typically > 20 pack years)
• Only 10-20% of smokers are affected
E-cigarettes??? PROBLEM WITH IT: not regulated thus not 100% safe right now…but still safer than smoking as it doesn’t have tar inside it….but stuff inside (or heat related) may affect the smoker anyways…
- As you get older, lung function decreases (% of FEV1)
- If lung function gets worse due to smoking: can be really fast (age 40) or slow (e.g. at 80)
- If lung function is getting worse with cigarettes and you stop: you don’t jump at to the same level as you would’ve been if you are a non-smoker at that age but you will assume the same rate of decline as if you are a non-smoker from that time= buy yourself time before you get to the threshold of breathlessness
mad
outline the main difference between asthma and COPD
asthma: reversible airways obstruction
copd: irreversible airways obstruction
• To get COPD: tend to need to smoke 20 cigarettes a day for 20 years
• “merger” box in the middle–> “asthma-COPD overlap syndrome”
• However, they may be partially reversible:
- Do spirometry
- Then give them salbutamol nebuliser or beta-2 agonist
- Re-do spirometry test 20 mins later
- May go from 70% to 77%
- Therefore, not enough to fit definition of reversibility associated with asthma but they got a bit better
outline the pathophysiological differences between asthma and COPD
Asthma: airway inflammation and hyperresponsiveness= bronchial muscle contraction= airway narrowing= REVERSIBLE
COPD: Alveolar destruction + airway inflammation= airway narrowing and reduced gas transfer= IRREVERSIBLE
The narrowing of COPD is irreversible and the drop in gas transfer is also irreversible
How can smoking cause COPD?
Alveolar macrophages recognise tar as if it’s a bug it has to kill thus releases proteases but can’t kill tar SO still active therefore digest other bits of protein around them (i.e. lung tissue)= destruction of collagen and elastase= emphysema.
This is one pathophysiological mechanism on how you get “holes” in the lung.
Around each alveolus is a blood vessel around it:
• Oxygen molecule can go into the capillary
• BUT if you wipe away some of the walls= end up with big air sacs
• = oxygen molecule has further to diffuse before it can get into blood vessel
how can you measure the degree of emphysema?
as it reduces oxygen absorption (through reducing the SA) = see reduced oxygen saturation–> gas transfer + walking (lose breath)
How is lung function measured?
- Spirometry–> FEV1/FEVC
- Gas transfer: take a big breath in of a gas (CO) that transfers well across the alveoli/capillary membrane–> hold breath for 10 secs and see how much CO is exhaled (Tells us how much gas absorption there is):
- Patients with reduced SA for gas transfer due to emphysema: spirometry is low
- Degree of emphysema can be seen by gas transfer: absorb less oxygen= reduced oxygen saturation= when you walk, muscles need more oxygen= lungs can’t deliver it= desaturate further when they walk
• Total lung volume
How can chronic bronchitis occur?
Paralysis of cilia + direct mucosal toxicity= Airway inflammation + mucus gland hyperplasia= Airway oedema + mucus hypersecretion= chronic bronchitis
- Cough up phlegm due to paralysis of cilia
- Cough to bring phlegm up
OUT OF BREATH DUE TO EMPHYSEMA
COUGH DUE TO CHRONIC BRONCHITIS
COPD
name the group of conditions related to COPD
Chronic bronchitis
Emphysema
Airways obstruction
define chronic bronchitis
Cough productive of sputum on most days for at least 3 months for 2 consecutive years
• Largely affects large/proximal airways
describe the pathophysiology of chronic bronchitis
– ↑ Goblet cells
– Mucus gland hypertrophy (=produce more mucus)
– Presence of mucus glands in smaller airways
– Bronchial wall inflammation
• Activated T-cells, macrophages, eosinophils, neutrophils
– Mucosal thickening
what are the symptoms of chronic bronchitis?
– Cough
– Sputum production
– Dyspnoea [BREATHLESSNESS] (esp on exertion)–> ASSOCIATED WITH/SIGNS–>
* Airflow obstruction (wheeze/prolonged expiration)
* Hypoxaemia
define emphysema
Abnormal permanent enlargement of distal airspaces accompanied by destruction of their walls without obvious fibrosis
describe the pathophysiology of emphysema
– alveolar wall destruction
– enlargement of distal airspaces
– loss of lung elastic recoil
normally: lots of alveoli with blood vessels running around
emphysema: breaking down holes until you get big “holes”
what are the symptoms of emphysema?
– progressive dyspnoea
– minimal cough/sputum
what are the signs of emphysema?
– Hyper-expansion (barrel chest)
– ↓ breath sounds
– Hypoxaemia
how can emphysema be measured?
• CT scanning • Pulmonary function testing – Increased residual volume: See total lung capacity. If exhale completely= don’t breathe all the gas out (known as residual volume which you can measure)
– Gas transfer reduces
• (TLCO/KCO)
describe airways obstruction
═ ↑ resistance to airflow caused by airway narrowing
- Combination of:
- Large airway disease
- Mucosal inflammation → bronchoconstriction
- Intra-luminal mucus
- Smooth muscle hypertrophy
- Small airway disease
- above
- Loss of outward traction on airways due to alveolar destruction
Due to combined effects of chronic bronchitis + emphysema
describe airway obstruction in emphysema
INSPIRATION IN AN EMPHYSEMA LUNG:
• Doesn’t make a difference as pushing whole chest wall open due to poor alveolar support
EXSPIRATION IN NORMAL LUNG VS EMPYSEMA LUNG:
• Normal lung: lots of alveoli attachments attached to chest wall to keep chest the same size
• COPD: fewer springs pulling airway open–>narrow airways–> goes to a smaller state….
Airways collapse–> can’t exhale fully–> more air in chest= increased residual volume= hard to get more air in= tidal volume increases = GET DYSPNOEIA
How can you measure airway obstruction?
• Spirometry
– FEV1
– FVC
– FEV1 / FVC ratio
– ↓ FEV1 (<70 % pred) & FEV1/FVC < 0.7 indicates obstructive disease
- Doesn’t really change after taking bronchodilators (beta 2 agonist)
HOW DO WE MEASURE WHETHER CHANGES ARE REVERSIBLE?
–>
Reversible testing
• Measurement of FEV1 pre and post bronchodilator
- Significant reversibility if >15% improvement
what is dyspnoea?
• Abnormal/uncomfortable awareness of breathing
– Sensation of increased drive to breath
• ↑ respiratory rate
• ↑ in tidal volume
– Sensation of inability to breath in or out
why are patients with COPD dyspnoeic?
• Airflow obstruction → impaired alveolar ventilation → air-trapping= “Barrel chest” • Impaired gas transfer → due to ↓ surface area for gas exchange → low oxygen level • Hyperinflation → Big breath in then little breath on top= not getting as much gas exchange (O2 in + CO2 out) → impaired alveolar ventilation
Why do patients with COPD have “barrel” chests?
= Residual volume being high in the chest
describe hyperinflammation in COPD
Emphysema + small airway narrowing (loss of elastic recoil, loss of traction on airways by alveolar structure)—> ariway collapse during expiration (loss of alveolar pressure exceeds airway pressure)–> Gas trapping–> increasing AP chest diameter
why do patients with COPD purse their lips to breathe?
Pursed lips increase the resistance to the outflow of air= prevention of airway collapse (increase in airway pressure)= increased air can be expired= increased ability to inspire fully
why are patients with COPD hypoxemic?
decreased surface area for gas exchange
what are the consequences of hypoxaemia?
• Pulmonary vasoconstriction
– pulmonary hypertension
– right heart strain and failure
• Increased erythropoietin production
– Increased red cells (polycythaemia)
– Increased haematocrit and viscosity
– Increased risk of stroke etc
how can stable COPD be managed?
Stop smoking?
• Bronchodilators – ↓ symptoms – ↑ exercise tolerance – Relaxation of airway smooth muscle – ↓ airway resistance – ↓ hyperinflation • Start with short acting drugs and progress to long acting if symptoms are not controlled • β2 agonists e.g/ Salbulatmol/ Terbutaline/Salmeterol
• Anticholinergics
e.g. Ipratropium/Tiotropium
- Theophyllines e.g. Aminophylline
- Corticosteroids
• Inhaled
– For all patients with FEV1 < 50% pred or 2 or more exaccerbations
• Oral
– For those with disease unresponsive to other measures
• Oxygen – Short burst – symptomatic – LTOT – 16 hours/day if PaO2 < 7.3 – Vaccinations – Influenza & Pneumococcus – Mucolytics • Palliation – Opiates & benzodiazepines • Pulmonary rehabilitation
