Chronic obstructive pulmonary disease Flashcards

1
Q

Define chronic obstructive pulmonary disease (COPD)

A

COPD = progressive airway disorder characterised by airway obstruction with little or no reversibility

Two types/underlying pathologies – most patients develop varying combinations on a spectrum

Chronic bronchitis
o Inflammation of the lining of bronchiole tubes
o Defined clinically as coughing and sputum production on most days for 3 months of 2 successive years

Emphysema
o Damage to the inner walls of the alveoli causes them to rupture
o Defined histologically as enlarged air spaces distal to the terminal bronchioles, with destruction of alveolar walls

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2
Q

How is the severity of COPD classified?

A

Using FEV1/FVC, given FEV1% compared to expected for age, size etc.

  • Mild = >80% of predicted
  • Moderate = 50-80% of predicted
  • Severe = 30-50% of predicted
  • Very severe = <30% of predicted
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3
Q

Explain the aetiology of COPD.

A

Tobacco smoke is the main cause
80% of COPD patients have significant smoking history
20% of smokers develop COPD

Tobacco smoke damages the lungs

  • Activates inflammatory cells
  • Oxidative stress
  • Impairs mucociliary clearance

Emphysema
In COPD, there is a protease-antiprotease imbalance, with excess neutrophil elastases destroying alveolar attachments
o Airways collapse as the alveolar septa are destroyed
o Compliance is increased (reducing elastic recoil and trapping air) causing a ventilation-perfusion mismatch
o Bullae (dilated air spaces >10mm) form – and may cause pneumothoraces

Mucus hypersecretion
o Obstruction occurs - Intraluminal mucus plugs, mucosal oedema, SM hypertrophy, fibrosis
o Bacteria can colonise the mucus

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4
Q

Explain the risk factors for COPD.

A

Smoking

Age (>40)

Environmental - Occupational dusts, Pollutants (outdoor and indoor biomass fuel usage)

Genetic
Alpha-antitrypsin-1 deficiency (2% - rare)
AAt = serum acute phase protein produced in liver which acts as a antiprotease in lung
AD inheritance
Suspected in COPD patients under 40 years old
Also have GI symptoms: Cirrhosis, cholestatic jaundice

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5
Q

Summarise the epidemiology of chronic obstructive pulmonary disease

A

Prevalence of 5-15% in industrialised countries

Major cause of morbidity and mortality
o 2.5 million deaths worldwide annually
o 4th leading cause of death in Europe and US
o Predicted to become the 5th biggest cause of morbidity in 2020

More common in men and over 50s

Increasing prevalence in women

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6
Q

Recognise the presenting symptoms of chronic obstructive pulmonary disease

A
  • SOB
  • Chronic productive cough
  • Chest tightness
  • Wheezing
  • Frequent respiratory infections
  • Unintended weight loss - Associated with risk of lung cancer
  • Reduced exercise tolerance

During an exacerbation
• Increased SOB
• Increased cough + sputum purulence + volume
• Increased wheeze
• Increased fatigue + reduced exercise tolerance
• Fluid retention
• Acute confusion

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7
Q

Recognise the signs of chronic obstructive pulmonary disease (COPD) on physical examination

A

Hyperinflation
o Barrel chest
o Decreased cricosternal distance (<3cm)
o Decreased chest expansion

Hyper-resonant percussion

Auscultation
o Quiet breath sounds – due to hyperinflated lung -> reduced air movement
o Polyphonic wheeze
o Coarse crackles

Hypoxia
o Use of accessory respiratory muscles
o Tachypnoea
o Cyanosis

Tar staining

RV HF
o Cor pulmonale
o Oedema
o Basal crepitations

Hypercapnia
o Vasodilation (long cap refill)
o Bounding pulse
o CO2 retention tremor

Pursing lips on expiration
o Due to increased PEEP

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8
Q

Identify appropriate investigations for chronic obstructive pulmonary disease

A

Spirometry = GOLD STANDARD
o TLC increased
o RV increased

Pulse oximetry

ABG - Decreased PaO2 , +/- hypercapnia

Bloods
o FBC - Raised PCV (polycythaemia)
o AAt (if <40 years old)

Sputum culture

CXR
o	Hyperinflation - >6 anterior ribs seen above diaphragm in MCL
o	Flat hemidiaphragms
o	Large central pulmonary arteries
o	Decreased peripheral vascular markings
o	Bullae
o	Elongated cardiac silhouette

ECG
o RAD
o RV hypertrophy
o Cor pulmonale

CT
o Bullae –> pneumothorax risk

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9
Q

Generate a management plan for chronic obstructive pulmonary disease

A

STOP SMOKING

Bronchodilators
Short acting beta 2 agonists (e.g. salbutamol)
Anticholinergics (e.g. ipratropium bromide)
Longacting beta 2 agonis ts (if > 2 exacerbations per year)
Steroids - Inhaled beclamethasone considered in all patients with FEV1 < 50% of predicted OR > 2 exacerbations per year

Regular oral steroids should be avoided if possible

Pulmonary rehabilitation

Oxygen therapy Only for those who stop smoking
Indicated if:
PaO2 < 7.3 kPa on air during a period of clinical stability
PaO2: 7.3-8 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension

Prevention of infective exacerbations: pneumococcal and influenza vaccination

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10
Q

How do you manage acute COPD exacerbation?

A

24% O2 via Venturi mask
Increase slowly if no hypercapnia and still hypoxic (do an ABG)
Corticosteroids
Start empirical antibiotic therapy if evidence of infection
Respiratory physiotherapy to clear sputum
Non-invasive ventilation may be necessary in severe cases

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11
Q

What are the potential complications of COPD?

A
Acute respiratory failure
Infections
Pulmonary hypertension
Right heart failure
Pneumothorax (secondary to bullae rupture)
Secondary polycythaemia
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12
Q

Summarise the prognosis for patients with COPD

A

High level of morbidity

BODE index - 4 year survival prediction
o Factors - BMI, Obstruction (FEV1 after bronchodilator), Dyspnoea, Exercise (distance walked in 6 minute)
o 0-2 points = 80%, 7-10 points = 18%

Most patients die from comorbidities – e.g. MI

Exacerbations have poor prognosis
o Readmission is common (70% in 1 year)
o 25% do not regain original peak flow 1 month later

Hypoxaemia (PaO2 < 8kPa) has a 5YS of less than 50%
o Supplemental O2 reduces mortality

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