COPD Flashcards

1
Q

Define COPD

A

A disease characterised by persistent respiratory symptoms and airflow limitation

Due to airways and/ or alveolar abnormalities

Caused by significant exposure to noxious particles or gases e.g. smoking 90%

Not one disease but a syndrome, number of distinct pathologies usually co-exist (often emphysema &/or chronic bronchitis)

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2
Q

Aetiology of COPD

A

smoking 90%

Air pollution

Biomass exposure - especially rural India/ China

Genetic (alpha 1 antitrypsin) <1% accelerated emphysema

Illicit drug use (smoking heroin/ weed) accelerated emphysema

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3
Q

How common is COPD?

A

Very, third biggest killer worldwide

2% of UK prevalence - increasing each year

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4
Q

Pathophysiology of COPD

A

Small airways disease (airway inflammation, airway fibrosis, luminal plugs, increased airway resistance)

——>

Parenchymal destruction (loss of alveolar attachments, decrease of elastic recoil)

——->
Airflow limitation

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5
Q

COPD: symptoms, risk factors, diagnosis

A

Symptoms: Dyspnoea worse exercise & progressive, chronic cough may intermittent/ unproductive, recurrent wheeze, chronic sputum, recurrent LRTIs

Risk factors: host factors e.g. genetic/ congenital, tobacco, occupation e.g. steal workers, indoor/ outdoor pollution, FH, low birthweight, childhood respiratory infections

Use both to assess then:

Spirometry - required to establish diagnosis

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6
Q

How do we measure the severity of COPD?

A

MRC dyspnoea scale :

Grades 1-5

MRC grade 1 - breathless with strenuous exercise

2 - short of breath when hurrying on the level or walking up a slight hill

3 - walk slower than ppl of the same age on the level bc of breathlessness or have to stop for breath when walking on their own pace on the level,

4 - stop for breath after walking 100m or after few minutes on level

5 - too breathless to leave house/ breathless when (un)dressing

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7
Q

Clinical signs of COPD

A

Often few or none especially at rest

  • clinical observation and on exertion
  • pursed lips breathing
  • hyperinflation/ barrel- shaped chest
  • prolonged expiratory phase

May have wheeze on auscultation

In advanced cases: cyanosis rarely, cor pulmonale (right sided heart failure) e.g. peripheral oedema/ raised JVP

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8
Q

How can we use spirometry to diagnose COPD?

A

takes deep breath in and blows as hard as possible into tube

Use spirometer volume/ time graph

Obstructive disease: FEV1 will be reduced more than vital capacity (takes longer to expire) FEV1: FVC reduced

Be cautious FEV1 varies with age

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9
Q

How can we use spirometry to measure severity of airflow obstruction?

A

Classification of airflow limitation severity in COPD (based on post- bronchodilator FEV1)

In patients with FEV1/ FVC <0.7:

GOLD 1 - mild FEV1 _> 80% of predicted

GOLD2 - moderate FEV1 _<50%, <80% predicted

GOLD3 - severe FEV1 _<30%, <50% predicted

GOLD 4 - very severe FEV1 <30% predicted

Severity of airflow obstruction NOT COPD

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10
Q

What other investigations can you carry out for COPD as well as spirometry?

A

Chest X–ray:
Not diagnostic, May suggest hyperinflation, mandatory to exclude other diagnoses e.g. cancer

High-resolution computed tomography:
Detailed assessment of the degree of emphysema, if suspicion of bronchiectasis, not required for routine assessment

Full pulmonary function tests:
Static lung volumes can assess for hyperinflation, gas transfer to look at alveolar destruction

Arterial blood gas:
If suspicion of respiratory failure e.g. SpO2 <92%

Alpha-1 antitrypsin blood test:
Younger patients/ atypical lower lobe emphysema

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11
Q

Exacerbations of COPD definition, how common, mortality

A

An acute worsening of respiratory symptoms that result in additional therapy (over day to day variability)

Very vague definition

Second most common cause of admission and highest cause of readmission

11.9% mortality at 90 days
43% readmitted at 90 days
Once admitted for COPD exacerbations

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12
Q

Which patients are most at risk of exacerbations?

A
  • previous exacerbations
  • disease severity (airflow obstruction and MRC dyspnoea score)
  • gastro-oesophageal reflux
  • pulmonary hypertension
  • respiratory failure
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13
Q

Aetiology of exacerbations

A
  • common bacteria 30%
    E.g. haemophilus influenza, streptococcus pneumoniae, moraxella catarrhalis. (20-30% pts chronically colonised)
  • common viral pathogens 23% e.g. rhinovirus, influenza

B + V = 25%

None = 31%

  • Atypical organisms e.g. mycoplasma pneumoniae, chlamydia spp
  • environmental factors e.g. pollution
  • eosinophilic e.g. eosinophils modulate type 2 mainly inflammatory pathway ✅ steroids
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14
Q

Therapies that improve symptoms & risk

A

symptoms:

  • pulmonary rehabilitation*
  • bronchodilators (beta 2 agonists LABA/ SABA & anti-muscurinics LAMA/ SAMA)
  • mucolytics (thin phlegm)
  • refractory dyspnoea management (low dose opiates, airflow therapy, CBT/ psychological input)
  • lung volume reduction surgery*
  • lung transplant*
  • palliative care

Risk:

  • smoking cessation*
  • O2 therapy (long term or ambulatory*)
  • anti- inflammatories* (inhaled corticosteroids, long term macrolides)
  • non- invasive ventilation (type 2 resp failure)
  • flu vaccine (best value non-pharmacological)
  • used for both
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15
Q

How does quitting smoking change your FEV1 and management of COPD?

A

Doesn’t improve it but slows worsening (so rate of decline goes back to similar levels as non-smoker but from a lower starting point)

Reduces mortality, improves symptoms, slows down loss of lung function, reduces exacerbations, drugs work better

Champix reduces addiction

As ciliary regrowth night get more cough & sputum short-term

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16
Q

What is pulmonary rehabilitation?

A

Exercise:
6-8 week course, hospital/ community, 2 supervised sessions/ week + 1 unsupervised, education, ongoing plan/ referral

83% some improvement

17
Q

Compare the bronchodilators beta-2 agonists & muscarinic antagonists in COPD

A

Muscarinic receptors in proximal airways, inhibit bronchoconstriction effect of AcH at M3 R smooth muscle, nonselective so also block M2 & M1

B2- adrenergic receptors more in distal airways, activate B2 R bronchioles -> increased cAMP-> relaxation SM

Increase airway calibre, reduce breathlessness & exacerbation

Long acting: used one or twice a day

18
Q

What effects do ICS have on inflammatory cells in bronchoalveolar lavage studies?

A

Reduced neutrophil and lymphocyte counts

Increased macrophage counts

No significant effect on eosinophils

in bronchoalveolar lavage studies

19
Q

What effects do ICS have on inflammatory cells in bronchial biopsies?

A

Reduced CD8+, CD4+ lymphocytes

No significant effects on neutrophils, eosinophils and CD68 macrophage counts

20
Q

What effect do inhaled corticosteroids have on exacerbations?

A

25% reduction

21
Q

When and why is long term O2 therapy used?

A

If someone is persistently hypoxic, non-smokers who don’t retain high levels of CO2 (as can lead to hypercapnia)
PO2 <7.3 KPa at rest (or <8KPa if cor pulmonale)

Extended hypoxaemia cause end-organ damage to heart and kidneys

Improves survival

Minimum 16hrs/ day

Safety- home fire risk assessment

22
Q

When is ambulatory O2 used and what does it do?

A

Reduces symptoms

If patients desaturate when walking (>4%), use during exertion

Need to walk further on O2, no prognostic benefit

23
Q

How to treat severe exacerbations

A

Hospitalisation - 12% mortality/ 43% readmitted at 3months

Bronchodilators - May nebulised therapy (SABA & SAMA) inhaled directly into lungs mask

Oral corticosteroids - prednisolone 5 days, in future may be based on blood eosinophil count

Controlled O2 if at risk type 2 resp failure - SpO2 88-92% , arterial blood gas

Antibiotics if indicated e.g. CRP/ WBCs raised/ symptoms

Wider therapy - inhaler technique, post pulmonary rehabilitation, smoking cessation

24
Q

What is non-invasive ventilation and what is it’s function?

A

Breathing support through a face/ nasal mask - air usually with added O2 given under positive pressure, generally altered depending if inhaling or exhaling

Tidal volume directly proportional to initial inspiratory positive airway pressure (IPAP)

Increased IPAP -> inc tidal volume -> inc minute volume -> dec CO2

Support ventilation and improve ventilatory function, reduce PaCO2 and raise PaO2, improve symptoms, increase life expectancy, reduced hospitalisation