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YR3 Respiratory > Obstructive lung disease: COPD, bronchiectasis, obstructive sleep apnoea > Flashcards

Obstructive lung disease: COPD, bronchiectasis, obstructive sleep apnoea Flashcards

1
Q

Define COPD

A

Chronic, progressive lung disorder characterised by airflow obstruction, with little/no reversibility.

Encompasses both emphysema and chronic bronchitis

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2
Q

What are the parameters for COPD?

A
  • FEV1:FVC ratio <0.7
  • FEV1 <80% of predicted
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3
Q

How are the 2 components of COPD (chronic bronchitis + emphysema) defined?

A

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

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4
Q

Explain the hallmark aetiology/pathophysiology of COPD

A

The hallmark of COPD is chronic inflammation from environmental toxins affecting:

  • both central and peripheral airways
  • lung parenchyma
  • alveoli
  • pulmonary vasculature

This causes:

  1. Resistance to airflow in small conducting airways due to narrowing, remodelling + fibrosis
    • → air trapping + increased lung compliance.
  2. Increased mucus- goblet cell hyperplasia + mucus gland hypertrophy
    • mucus plugging leads to infections
    • increased mucus also leads to obstruction
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5
Q

What are the core cells in the pathogenesis of COPD? How do these cells affect the alveoli?

A

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
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6
Q

How does COPD leads to pulmonary hypertension?

A

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
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7
Q

Summarise the epidemiology of COPD

A
  • 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
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8
Q

WHat are the presenting symptoms of COPD?

A
  • SOB/dyspnoea typically persistent and over time
  • Chronic recurrent cough
    • initially presents in morning
  • Regular sputum production
  • Frequent LRTI
  • Wheeze
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9
Q

List the clinical signs of COPD

A
  • 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)
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10
Q

What are the signs of CO2 Retention ?

A
  • Bounding pulse
  • Warm peripheries
  • Asterixis
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11
Q

What is the gold standard test for COPD?

A

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.

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12
Q

What investigations would you do for COPD?

A
  • 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
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13
Q

State some signs of hyperinflation on CXR

A
  • > 6 anterior ribs
  • flattened hemidiaphragm
  • Increased anteroposterior ratio
  • increased intercostal spaces
  • hyperlucent lungs (blacker than normal)
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14
Q

Describe the general advice/non-pharmacoloigcalmanagement for stable COPD

A

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
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15
Q

Outline the BTS guidelines for the treatment of COPD

A
  1. Initiate SABA (salbutamol)/SAMA (ipratropium)

Then:

  1. If FEV1>50%:
    • LABA (salmeterol)
      • or LAMA (tiotropium)
    • If worsens: add ICS to LAMA/LABA
  2. If FEV1 <50%:
    • LABA+ICS (beclomethasone) in combined inhaler
      • or LAMA
    • If worsens: add ICS to LABA/ICS combo
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16
Q

How are acute exacerbations of COPD managed?

A

Note: usually occurs in winter due to viral/bacterial infections

  1. Controlled O2 therapy using 24% Venturi Mask aiming for sats at 88-92%.
    • Adjust according to ABG, aiming PaO2 >8kPa
  2. 5mg nebulised salbutamol +
  3. 0.5mg nebulised ipratropium +
  4. 200mg IV hydrocortisone
    • OR 40mg PO prednisolone
  5. Then: 500mg/8hr amoxicillin
  6. If no improvement: IV aminophylline
  7. If no improvement: biphasic NIV (BiPAP)
  8. If no improvement: intubation and ventilate in ICU
17
Q

Identify the possible complications of COPD

A
  • Acute respiratory failure
  • Infections
  • Pulmonary hypertension
  • Right heart failure
  • Pneumothorax (secondary to bullae rupture)
  • Secondary polycythaemia
18
Q

Summarise the prognosis for patients with COPD

A
  • 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
19
Q

Define bronchiectasis

A

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

20
Q

Explain the aetiology of bronchiectasis

A

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
21
Q

Explain the pathophysiology of bronchiectasis

A

Viscious cycle

  1. Initial aetiological insult + primary infection → increased inflammation → bronchial damage, dilation + thickening
  2. Damage predisposes to persistent bacterial colonisation
  3. → chronic inflammatory reaction
  4. Eventually leads to progressive airway damage and recurrent infections.
25
Q

What investigations would you do for bronchiectasis?

A
  • 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
26
Q

Summarise the epidemiology of bronchiectasis

A
  • Incidence has decreased with the use of antibiotics
  • 1/1000 per year
  • more common with advancing age
27
Q

How is bronchiectasis managed?

A
  1. Advice on healthy diet + exercise
  2. Airway clearance therapy
    • maintain hydration
    • postural drainage- 2-3x daily. unpleasant
    • chest physiotherapy
    • clears sputum + mucus
  3. Inhaled bronchodilator
    • salbutamol, ipratropium
    • nebulised in acute attack
  4. Nebulised hypertonic saline
    • mucoactive agent, reduces inflammation
  5. Short-term oral or IV antibiotic
    • in acute exacerbations
    • with coverage based on sputum culture
  6. Surgery
    • In localised disease refractory to medical Tx or massive haemoptysis
    • resection of focal bronchiectatic area
    • lung transplant in under 65s
28
Q

What are the presenting symptoms of bronchiectasis?

A

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

29
Q

State some signs of bronchiectasis O/E

A
  • 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
31
Q

State some common pathogens found in sputum C+S for bronchiectasis

A

Common organisms:

  • Pseudomonas aeruginosa
  • Haemophilus influenzae
  • Staphylococcus aureus
  • Streptococcus pneumoniae
  • Klebsiella
  • Mycobacteria
  • Aspergillus
33
Q

What are the complications of bronchiectasis?

A
  • Life-threatening haemoptysis
  • Pneumonia
  • Pneumothorax
  • Persistent infections
  • Empyema
  • Respiratory failure
  • Cor pulmonale
  • Multi-organ abscesses
  • Amyloidosis
34
Q

Summarise the prognosis for patients with bronchiectasis

A

Most patients continue to have symptoms after 10 years

35
Q
A
36
Q

Define obstructive sleep apnoea

A

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

37
Q

Explain the pathophysiology of obstructive sleep apnoea

A
  • 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
38
Q

What are the RF for OSA?

A
  • 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)
39
Q

Summarise the epidemiology of obstructive sleep apnoea

A
  • COMMON
  • 5-20% of men > 35 yrs
  • 2-5% of women > 35 yrs
  • Prevalence increases with age
40
Q

Recognise the presenting symptoms of obstructive sleep apnoea

A
  • 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
41
Q

What appropriate investigations for obstructive sleep apnoea ​

A

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

42
Q
A

YR3 Respiratory (6 decks)

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