Chronic obstructive airways disease Flashcards

1
Q

Chronic obstructive airways disease

A

Please examine this patient’s chest; he has a chronic chest condition.

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2
Q

Clinical signs

A
  • Inspection: nebulizer/inhalers/sputum pot, dyspnoea, central cyanosis and pursed lips
  • CO2 retention flap, bounding pulse and tar‐stained fingers
  • Hyper‐expanded
  • Percussion note resonant with loss of cardiac dullness
  • Expiratory polyphonic wheeze (crackles if consolidation too) and reduced breath sounds at apices
  • Cor pulmonale: raised JVP, ankle oedema, RV heave; loud P2 with pansystolic murmur of tricuspid reurgitation
  • COPD does not cause clubbing: therefore, if present consider bronchial carcinoma or bronchiectasis
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3
Q

Discussion of COPD

A
  • Spectrum of disease with airway obstruction (with or without sputum production); can be low FEV1 at one end and emphysema with low O2 sats but normal spirometry at the other
  • Degree of overlap with chronic asthma, although in COPD there is less reversibility (<15% change in FEV1 post‐bronchodilators)
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4
Q

Causes of COPD

A
  • Environmental: smoking and industrial dust exposure (apical disease)
  • Genetic: α1‐antitrypsin deficiency (basal disease)
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5
Q

Investigations for COPD

A
  • CXR: hyper‐expanded and/or pneumothorax
  • ABG: type II respiratory failure (low PaO2 high PaCO2)
  • Bloods: high WCC (infection), low α1‐antitrypsin (younger patients/FH+), low albumin (severity)
  • Spirometry: low FEV1, FEV1/FVC < 0.7 (obstructive)
  • Gas transfer: low TLCO
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6
Q

Treatment of COPD

A
  • Medical – depends on severity (GOLD classification):
    ⚬⚬ Smoking cessation is the single most beneficial management strategy
    ⚬⚬ Cessation clinics and nicotine replacement therapy
    ⚬⚬ Long‐term oxygen therapy (LTOT)
    ⚬⚬ Pulmonary rehabilitation
    ⚬⚬ Mild (FEV1 >80) – beta‐agonists
    ⚬⚬ Moderate (FEV1 <60%) – tiotropium plus beta‐agonists
    ⚬⚬ Severe (FEV1 <40%) or frequent exacerbations -above plus inhaled corticosteroids; although avoid if patient has ever had an episode of pneumonia (TORCH trial)
    ⚬⚬ Exercise
    ⚬⚬ Nutrition (often malnourished)
    ⚬⚬ Vaccinations ‐ pneumoccoal and influenza
  • Surgical (careful patient selection is important)
    ⚬⚬ Bullectomy (if bullae >1 L and compresses surrounding lung)
    ⚬⚬ Endobronchial valve placement
    ⚬⚬ Lung reduction surgery: only suitable for a few patient with heterogeneous distribution of emphysema
    ⚬⚬ Single lung transplant
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7
Q

LONG-TERM OXYGEN THERAPY (LTOT )

A
  • Inclusion criteria:
    ⚬⚬ Clinically stable, Non‐smoker with PaO2 <7.3 kPa on air despite max Rx –> Value should be measured on 2 different occasions 3 weeks apart
    ⚬⚬ If PaO2 7.3-8 Kpa + evidence of cor pulmonale, pulmonary HTN, polythycemia, or nocturnal hypoxia
    ⚬⚬ PaCO2 that does not rise excessively on O2
    ⚬⚬ For terminally ill patients
  • 2–4 L/min via nasal prongs for at least 15 hours a day
  • Improves average survival by 9 months
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8
Q

Treatment of an acute exacerbation

A
  • Controlled O2 via Venturi mask monitored closely
  • Bronchodilators
  • Antibiotics
  • Steroids 7 days
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9
Q

Prognosis

A

COPD patients with an acute exacerbation have 15% in‐hospital mortality

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10
Q

Differential of a wheezy chest

A
  • Granulomatous polyarteritis (previously Wegner’s): saddle nose; obliterative bronchiolitis
  • Rheumatoid arthritis: wheeze secondary to obliterative bronchiolitis
  • Post‐lung transplant: obliterative bronchiolitis as part of chronic rejection spectrum
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