Obstructive lung disease: COPD, bronchiectasis, obstructive sleep apnoea Flashcards
Define COPD
Chronic, progressive lung disorder characterised by airflow obstruction, with little/no reversibility.
Encompasses both emphysema and chronic bronchitis
What are the parameters for COPD?
- FEV1:FVC ratio <0.7
- FEV1 <80% of predicted
How are the 2 components of COPD (chronic bronchitis + emphysema) defined?
CHRONIC BRONCHITIS- defined clinically
chronic cough and sputum production on most days for at least 3 months per year for 2 consecutive years
EMPHYSEMA- defined histologically
permanently dilated airspaces distal to the terminal bronchioles, with destruction of alveolar walls
Explain the hallmark aetiology/pathophysiology of COPD
The hallmark of COPD is chronic inflammation from environmental toxins affecting:
- both central and peripheral airways
- lung parenchyma
- alveoli
- pulmonary vasculature
This causes:
-
Resistance to airflow in small conducting airways due to narrowing, remodelling + fibrosis
- → air trapping + increased lung compliance.
-
Increased mucus- goblet cell hyperplasia + mucus gland hypertrophy
- mucus plugging leads to infections
- increased mucus also leads to obstruction
What are the core cells in the pathogenesis of COPD? How do these cells affect the alveoli?
Activated macrophages, neutrophils, and leukocytes
Oxidative stress and an excess of proteases amplify the effects of chronic inflammation
- Proteases break down elastin and collagen, meaning alveoli permanently enlarge and lose recoil elasticity
- This forms bullae + airways that collapse inwards on inspiration
- airways are more compliant- so fill up but air has dfficulty leaving → air trapping
How does COPD leads to pulmonary hypertension?
Hyperinflation and destruction of lung parenchyma predispose patients with COPD to hypoxia, particularly during activity.
Progressive hypoxia causes:
- vascular smooth muscle thickening to shunt blood to from hypoxic areas to those with better exchange
- As a large proportion of the lungs are not well perfused this leads to increased vascular resistance
Summarise the epidemiology of COPD
- VERY COMMON (8% prevalence)
- Presents in middle age or later
- More common in males - this may change because there has been a rise in female smokers
WHat are the presenting symptoms of COPD?
- SOB/dyspnoea typically persistent and over time
-
Chronic recurrent cough
- initially presents in morning
- Regular sputum production
- Frequent LRTI
- Wheeze
List the clinical signs of COPD
-
Barrel chest
- due to hyperinflation and air trapping 2/2 incomplete expiration
-
Pursed lip breathing
- prolongs expiration and decreases air trapping
-
Hyperresonant on percussion
- due to hyperinflation + air trapping
- on auscultation:
- course crepetations- due to mucus hypersecretion. DISCONTINUOUS
- reduced breath sounds- loss of lung elasticity + tissue breakdown → poor air movement
- wheeze- indicates increased airway resistance due to inflammation. CONTINUOUS, MUSICAL
-
cachexia
- 2/2 increased work due to tachypnoea + accessory muscle use + anorexia
- tachypnoea + use of accessory muscles
-
congested neck veins
- 2/2 increased intrathoracic pressure and cor pulmonale
-
asterixis
- due to hypercapnoea 2/2 impaired gas exchange
Advanced disease (2/2 cor pulmonale (RHF)):
- hepatosplenomegaly
- cyanosis
- Loud P2 (second heart sound)
What are the signs of CO2 Retention ?
- Bounding pulse
- Warm peripheries
- Asterixis
What is the gold standard test for COPD?
Spirometry and Pulmonary Function Tests
Test establishes FEV1 and FVC. The ratio of these two values indicates whether airflow obstruction is present.
- Reduced PEFR
- FEV1/FVC ratio <0.70
- Increased lung volumes
Spirometry should be performed after administering an adequate dose of at least one short-acting inhaled bronchodilator to minimise variability.
What investigations would you do for COPD?
- Spirometry
-
Pulse oximetry/ABG
- SaO2 of 88-90% may be acceptable.
- CO2 may be raised
-
CXR
- signs of hyperinflation
- FBC
- raised haematocrit (polycythaemia)
- anaemia
- leukocytosis esp in acute exacerbation
- ECG
- signs of right ventricular hypertrophy, arrhythmia, ischaemia
- RF for IHD = RF for COPD (often coexist)
-
Pulmonary function tests
- obstructive pattern
- decreased DLCO- diffusing capacity of the lung for carbon monoxide- shows emphysema
-
CT chest
- Provides better visualisation of type and distribution of lung tissue damage and bulla formation than CXR.
-
sputum culture
- In patients with frequent exacerbations/ severe airflow limitation
State some signs of hyperinflation on CXR
- > 6 anterior ribs
- flattened hemidiaphragm
- Increased anteroposterior ratio
- increased intercostal spaces
- hyperlucent lungs (blacker than normal)
Describe the general advice/non-pharmacoloigcalmanagement for stable COPD
MDT approach to help patients with:
- Stop smoking
- Encourage exercise
- Treat poor nutrition or obesity
- Influenza and pneumococcal vaccination
- Pulmonary rehabilitation/palliative care- includes LTOT
- Psychiatric support
- “Rescue pack”- course of Abx to use only in case of acute exacerbations
Outline the BTS guidelines for the treatment of COPD
- Initiate SABA (salbutamol)/SAMA (ipratropium)
Then:
-
If FEV1>50%:
-
LABA (salmeterol)
- or LAMA (tiotropium)
- If worsens: add ICS to LAMA/LABA
-
LABA (salmeterol)
-
If FEV1 <50%:
-
LABA+ICS (beclomethasone) in combined inhaler
- or LAMA
- If worsens: add ICS to LABA/ICS combo
-
LABA+ICS (beclomethasone) in combined inhaler
How are acute exacerbations of COPD managed?
Note: usually occurs in winter due to viral/bacterial infections
- Controlled O2 therapy using 24% Venturi Mask aiming for sats at 88-92%.
- Adjust according to ABG, aiming PaO2 >8kPa
- 5mg nebulised salbutamol +
- 0.5mg nebulised ipratropium +
-
200mg IV hydrocortisone
- OR 40mg PO prednisolone
- Then: 500mg/8hr amoxicillin
- If no improvement: IV aminophylline
- If no improvement: biphasic NIV (BiPAP)
- If no improvement: intubation and ventilate in ICU
Identify the possible complications of COPD
- Acute respiratory failure
- Infections
- Pulmonary hypertension
- Right heart failure
- Pneumothorax (secondary to bullae rupture)
- Secondary polycythaemia
Summarise the prognosis for patients with COPD
- High morbidity
- 3-year survival of 90% if < 60 yrs, FEV1 > 50% predicted
- 3-year survival of 75% if > 60 yrs, FEV1: 40-49% predicted
Define bronchiectasis
Permanent/chronic dilation of the bronchi due to destruction of the elastic and muscular components of the bronchial wall
Associated with impaired mucociliary clearance and recurrent bacterial infections
Explain the aetiology of bronchiectasis
Often caused as a consequence of recurrent and/or severe infections 2/2 an underlying disorder.
This causes permanent bronchial damage
- Idiopathic (50%)
-
Post-infectious (30%)
- severe aspergillosis
- childhood viral infections
- severe bacterial pneumonia
-
Immunodeficiency (5%)
- HIV
- Immunoglobulin deficiency
-
Genetic (3%)
- CF
- Ciliary dyskinesia
-
Inflammatory (5%)
- COPD
- asthma
- IBD
Explain the pathophysiology of bronchiectasis
Viscious cycle
- Initial aetiological insult + primary infection → increased inflammation → bronchial damage, dilation + thickening
- Damage predisposes to persistent bacterial colonisation
- → chronic inflammatory reaction
- Eventually leads to progressive airway damage and recurrent infections.
What investigations would you do for bronchiectasis?
- Bloods- WBC for infection (neutrophilia)
-
Sputum culture + sensitivity
- may be single or multiple pathogens present.
-
CXR
- not diagnostic but good for monitoring
- obscured hemidiaphragm
- dilated bronchi (seen as parallel lines from hilum → diaphragm = tramline shadows)
- Pneumonic consolidations
-
HRCT chest
- DIAGNOSTIC- see extent of disease
- dilation of bronchi + airway thickening
-
Spirometry
- usually shows obstructive image – should assess reversibility
-
Tests for aetioligical agent
- RF test
- serum a-1 anti-trypsin
- sweat chloride test
- Nasal Nitric Oxide (PCD test)
- skin prick test - aspergillus
Summarise the epidemiology of bronchiectasis
- Incidence has decreased with the use of antibiotics
- 1/1000 per year
- more common with advancing age
How is bronchiectasis managed?
- Advice on healthy diet + exercise
-
Airway clearance therapy
- maintain hydration
- postural drainage- 2-3x daily. unpleasant
- chest physiotherapy
- clears sputum + mucus
-
Inhaled bronchodilator
- salbutamol, ipratropium
- nebulised in acute attack
-
Nebulised hypertonic saline
- mucoactive agent, reduces inflammation
-
Short-term oral or IV antibiotic
- in acute exacerbations
- with coverage based on sputum culture
-
Surgery
- In localised disease refractory to medical Tx or massive haemoptysis
- resection of focal bronchiectatic area
- lung transplant in under 65s
What are the presenting symptoms of bronchiectasis?
History: CF, immunodeficiency, previous infections, aspiration, congenital airway disorders
-
Peristent cough with large amounts of purulent sputum
- worsened by lying flat
- sputum may be flecked with blood
-
Dyspnoea
- worse on exercise
-
Fever
- acute exacerbations
- recurrent + episodic
- Pleuritic chest pain
- weight loss, fatigue
Symptoms usually begin after an acute respiratory illness + worsen during acute exacerbations
State some signs of bronchiectasis O/E
- Clubbing
-
Coarse inspiratory crackles/crepitations (usually at lung bases)
- These shift with coughing
- Due to mucus
-
Wheeze – high-pitched inspiratory squeaks + pops
- due to bronchial obstruction/inflammation
State some common pathogens found in sputum C+S for bronchiectasis
Common organisms:
- Pseudomonas aeruginosa
- Haemophilus influenzae
- Staphylococcus aureus
- Streptococcus pneumoniae
- Klebsiella
- Mycobacteria
- Aspergillus
What are the complications of bronchiectasis?
- Life-threatening haemoptysis
- Pneumonia
- Pneumothorax
- Persistent infections
- Empyema
- Respiratory failure
- Cor pulmonale
- Multi-organ abscesses
- Amyloidosis
Summarise the prognosis for patients with bronchiectasis
Most patients continue to have symptoms after 10 years
Define obstructive sleep apnoea
Complete/partial episodic airway obstruction due to collapse of the pharyngeal airway during sleep, leading to apnoea (cessation of breathing>10s), followed by partial arousal
Explain the pathophysiology of obstructive sleep apnoea
- Upper pharyngeal dilator muscle activity decreases with sleep onset
- Most vulnerable to collapse at end expiration due to negative intraluminal pressure
- People with OSA have a narrow pharyngeal cross-sectional area + so they are vulnerable to apnoea
- Hypoxaemia and hypercapnia result from airway obstruction → arousal
What are the RF for OSA?
- Weight gain – soft tissue in neck area
- Surgical swelling
- Smoking
- Alcohol
- PCOS- combo of high androgenic hormones + obesity
- Sedative use
- Large neck circumference
- Enlarged tonsils and adenoids in children
- Macroglossia
- Marfan’s, Down’s syndrome
- Maxillomandibular anomalies (e.g., narrowing, retrognathia, and high, arched palate)
- Increased volume of soft tissues (includes tonsils, adenoids, and tongue)
Summarise the epidemiology of obstructive sleep apnoea
- COMMON
- 5-20% of men > 35 yrs
- 2-5% of women > 35 yrs
- Prevalence increases with age
Recognise the presenting symptoms of obstructive sleep apnoea
- Excessive daytime sleepiness
- Maxomandibular abnormalities- narrowing of jaw, overbite, overjet, malocclusion.
- Unrefreshing or restless sleep, insomnia
- Macroglossia
- Irritability and mood changes, decreased libido and cognitive performance
- Partner reporting:
- loud snoring
- nocturnal apnoeic episodes
- nocturnal choking
What appropriate investigations for obstructive sleep apnoea
Polysomnography- definitive test
- Monitor overnight with polysomnogram
- Monitor airflow, respiratory effort, pulse oximetry and heart rate and snoring and movement
- Occurrence of >15 episodes of apnoea/hypopnoea per hour indicates significant sleep apnoea
Other more simple tests measure less than polysomnography- used when very probable clinical diagnosis / no co-mobidities
Fibreoptic endoscopy- exclude nasal polyps/tumours or hypertrophic lingual tonsils
