Respiratory

Question 1

What is COPD and what causes it?

Answer 1

COPD - chronic obstructive pulmonary disorder is a disease state characterised by airflow limitation that is not fully reversible. It is however is a preventable and treatable.

• It encompasses both emphysema and chronic bronchitis.
• Although COPD affects the lungs, it also has significant systemic consequences e.g. exacerbations and comorbidities which contribute to the overall condition and prognosis in individual patients

The airflow limitation is usually progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases.

• It is primarily caused by tobacco smoking.
• responsible for 40% to 70% of COPD cases and exerts its effect by causing an inflammatory response, cilia dysfunction, and oxidative injury.
• Air pollution and occupational exposure are other common aetiologies.

Important factors in COPD pathogenesis:

• Oxidative stress and an
• imbalance in proteinases and antiproteinases
• especially in patients with alpha-1 antitrypsin deficiency, who have panacinar (uniform enlargement of airspaces throughout the terminal bronchioles and alveoli) emphysema that usually presents at an early age.
  
  • these are the ~10% who can get COPD without ever smoking

Question 2

What is the pathophysiology of COPD?

Answer 2

The hallmark of COPD:

• chronic inflammation that affects central airways, peripheral airways, lung parenchyma and alveoli, and pulmonary vasculature.
• inhaled stimuli –> inflammatory reaction responsible for the changes in the airways, alveoli, and pulmonary blood vessels.
  
  • The main components of these changes are:
    
    • narrowing and remodelling of airways,
    • increased number of goblet cells,
      
      • –> enlargement of mucus-secreting glands (contianing goblet cells) of the central airways
    • subsequent vascular bed changes leading to pulmonary hypertension.

Activated macrophages, neutrophils, and leukocytes are the core cells in this process.

• In contrast to asthma, eosinophils play no role in COPD, except for occasional acute exacerbations.

In COPD subtype - emphysema: inflammatory responses neutrophils –> elastases –> elastin breakdown and subsequent loss of alveolar integrity which means the terminal bronchioles cannot stay open.

• Decreased elastic recoil,

In chronic bronchitis, (another phenotype of COPD) these inflammatory changes (by inhaled substances) lead to ciliary dysfunction as to protect the airways there is squamous cell metaplasia (cilia have to be lost to do this) and this means defective mucocilary clearance! and also increased goblet cell size and number –> mucus gland hypersecretion.

• fibrotic changes in lung parenchyma
• luminal obstruction of airways by secretions

These changes cause:

• for decreased airflow (from increased airways resistance; the pysiological hallmark of COPD),
• hypersecretion,
• chronic cough.

In both conditions, changes are progressive and usually not reversible.

Expiratory flow limitation –> hyperinflation.

Hyperinflation + destruction of lung parenchyma, –> COPD patients to hypoxia, –> particularly during activity.

Progressive hypoxia –>vascular smooth muscle thickening –> pulmonary hypertension, which is a late development conveying a poor prognosis.

Question 3

What are the signs and symptoms of COPD?

Answer 3

COPD = insidious onset TF usually presents in older people.

A typical history =

• productive cough,
  
  • normally clear sputum
• wheezing, and
• shortness of breath,
  
  • particularly with exercise.

constant nocturnal cough

• fatigue

and persistent hypoxia and hypercapnia.

• headache
  
  • May occur due to vasodilation caused by hypercapnia.

infectious exacerbation:

• acute, severe shortness of breath,
• fever,
• chest pain

Determine: The patient’s

• smoking history,
• occupational exposures,
• family history of lung disease should be determined.

Physical examination may show:

• tachypnoea,
  
  • hypoxia compensation sign
• respiratory distress,
• use of accessory muscles,
• intercostal retraction.
• Barrel chest
  
  • hyper-resonance on percussion, and
  • distant breath sounds and
    
    • All of these are caused by air-trapping
  • poor air movement on auscultation
    
    • Secondary to loss of lung elasticity and lung tissue breakdown.
• Wheezing,
  
  • (coutninuous sound) Is indicative of airway inflammation and resistance. e.g. in exacerbations
• coarse crackles,
  
  • A common finding in exacerbations.
  • (discontinuous) sound referring to mucus or sputum in airways.
  • Indicative of airway inflammation and mucus over-secretion.
• clubbing,
  
  • COPD itself does not cause clubbing, but if tobacco exposure in COPD patients leads to lung cancer and/or bronchiectasis,
  • Clubbing = only after significant impairment of lung function has occurred.
• cyanosis,
• signs of right-sided heart failure [cor pulmonale]
  
  • (distended neck veins, loud P2 [pulmonic valve closure, e.g. S2], hepatomegaly, hepatojugular reflux, and lower-extremity oedema), may be present.
• Occasional = asterixis - loss of postural control in the outstretched arms (commonly known as a flap) caused by hypercapnia.
  
  • impaired gas exchange in lung parenchyma, worsens with exercise = respiratory failure.

Question 4

What are the investigations of COPD?

Answer 4

• Spirometry is the first test for diagnosis of COPD and for monitoring disease progress.
  
  • reduced FEV1 and FEV1/FVC ratio.
  • GOLD criteria define airflow limitation as a post-bronchodilator FEV1/FVC <0.70. [1]
• Chest x-ray (CXR)
  
  • exclude other diagnoses.
• Pulse oximetry screens for hypoxia.

Patients presenting with acute symptoms should have

• full blood count,
• ECG,
• chest x-ray, and
• assessment of gas exchange
  
  • pulse oximetry
    
    • If peripheral arterial oxygen saturation is less than 92%, then arterial or capillary blood gases should be measured. (RS HF or resp failure)
  • and/or ABG

Spirometry is not recommended in an acute exacerbation as it may be hard to perform and not very accurate.

Other tests

In an acute exacerbation,

• empirical antibiotics should be given if the patient has
• increase in dyspnoea,
• sputum volume, and
• sputum purulence;
  
  • if exacerbations are freqent, needs mech ventilation, airflow is severely limited –> send for culture

alpha-1 antitrypsin level should be checked. In young patients (<45 years) with a family history or with rapidly progressing disease and lower lobe changes on imaging tests,

CT scans show anatomical changes, patients considered for surgery and for ruling out other pathologies.

Exercise testing can be useful in patients with a disproportional degree of dyspnoea. & for selecting patients for rehabilitation.

Respiratory muscle function test if dyspnoea or hypercapnia are disproportionately increased w/r FEV1, as well as in patients with poor nutrition and those with corticosteroid myopathy.

Question 5

What is the management of COPD in chronic stable patients?

Answer 5

• Smoking cesation
• Patient education
  
  • pulmonary rehabilitation
• Encourage exercise
  
  • BMI is often low
• Diet advice -
  
  • protein is important if exercising as part of pulmonary rehab
• Mucolytics (to help chronic progressive cough)
• Treat depression (that may result from disabilities)
• Respiratory failure
• Diuretics for oedema
• Vaccinations –> flu and pneumococcal
• Long term oxygen therapy

In advanced COPD [use gold criteria and BODE index to identify severity]

1. Initiate short acting B2 agonist (SABA) or short acting muscarinic antagonist (SAMA)
   
   • SABA = ​Salbutamol inhaler,
   • SAMA = ipratropium
2. if FEV1 is over 50%
   
   • use a long acting B2 agonist (LABA)
     
     • salmeterol, indacterol (inhaled)
   • and a long acting muscarinic antagonist (LAMA)
     
     • tiotropium
   1. if still not good use LABA plus ICS
      
      • ICS [short course of oral] = prednisolone or methyprednisolone
   2. then use LAMA plus LABA/ICS combination inhaler
      
      • For transition to long term inhaled CS therapy -
        
        • beclometasone, budesonide
3. If FEV1 is under 50%
   
   • use a LABA PLUS inhaled corticosteroid [in combined inhaler]
     
     • beclometasone, budesonide
     • LABA = salmeterol, indacaterol
   • and a long acting muscarinic antagonist (LAMA)
     
     • Tiotropium, umeclidinium
   1. if not working use LAMA plus LABA/ICS combination inhaler

• Pulmonary rehabilitation
  
  • airway clearance techniques e.g.
• consider Long term oxygen therapy
  
  • non invasive ventilation if hypercapnic
• surgery - lung volume reduction; endobronchial valve; transplant
  
  • if recurrent pneumorthroaces
  • isolated bullous disease (autoimmune blisters in elderly)
• consider palliative care input
  
  • NB: air travel is risky if FEV1<50% or PaO2 <6.7kPa on air

Refer to specialist for:

• assessment of oral corticosteroids,
• nebuliser therpy or LTOT,
• frequent infecctions,
• cor pulmonale
  
  • or if less than 10 pack years smoking or under 40y/o (a-1t deficiency? –> has familial implications)
  • uncertain
  • Also if rapid FEV1 decline/severe COPD,
  • or for surgical assessment.

Question 6

What is the treatment of emergency COPD?

Answer 6

• nebulised SA bronchodilators
  
  • salbutamol or ipratropium
• Controlled o2 therapy if SaO2 <88% or paO2<7
• Steroids
  
  • hydrocortizone IV
  • oral prednisolone
    
    • transition to inhaled –> beclometasone
• Antibiotics
  
  • if evidence of infection - and cardinal symptoms of COPD: dyspnoea, sputum volume, sputum purulence
    
    • doxycycline, tetracycline, amoxicillin, [broad spectrum]
• Physio to air sputum expectoration/Airway clearance techniques
• if nebilisers and steroids dont work –> ?iv aminophylline (SA bronchidilator)

Question 7

How do you assess severity of COPD and what treatments do you give for the different severities?

Answer 7

FEV/FEV1 <0.7 confirms COPD, then:

The GOLD guideline uses a combined COPD assessment approach to group patients according to symptoms and previous history of exacerbations.

In addition to previous exacerbations, airflow limitation <50% is predictive of exacerbations.

Symptoms are assessed using the mMRC or CAT scale.

Group A: low risk

• >80%
• (0-1 exacerbation per year, not requiring hospitalisation) and
• fewer symptoms (mMRC 0-1 or CAT <10)
  
  • Any bronchodilator
    
    • Salbutamol (SABA)
    • Ipratropium (SAMA)
    • Salmeterol (LABA)
    • Indacaterol (LAMA)
• Patient education and vaccination; and smoking cessation

Group B:

• 50-79%
• low risk (0-1 exacerbation per year, not requiring hospitalisation) and
• more symptoms (mMRC≥ 2 or CAT≥ 10)
  
  • LABA or LAMA
  • Salmeterol or indacaterol (inhaled)
  • 2nd line Short acting bronchodilator as required
    
    • salbutamol or ipratropium
• Patient education and vaccination, smoking cessation + pulmonary rehab

Group C:

• 30-49%
• high risk (≥2 exacerbations per year, or one or more requiring hospitalisation) and
• fewer symptoms (mMRC 0-1 or CAT <10)
  
  • LAMA
    
    • Tiotropium, umeclidinium

Group D:

• <30%
• high risk (≥2 exacerbations per year, or one or more requiring hospitalisation) and
• more symptoms (mMRC≥ 2 or CAT≥ 10).
  
  • LAMA
    
    • tiotropium, umeclidinium
  • or LAMA and LABA
    
    • umeclidinium/vilanterol inhaled
    • glycopyrronium/formoterol fumarate
  • ICS and LABA
    
    • e.g. asthma COPD overlap
    • fluticasone furoate/vilanterol