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Respiratory > COPD and bronchiectasis > Flashcards

COPD and bronchiectasis Flashcards

1
Q

What is COPD characterised by?

A
  • Persistent respiratory symptoms
  • Airflow limitation
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2
Q

What is COPD?

A
  • Occurs due to airways and/or alveolar abnormalities
  • Caused by significant exposure to noxious particles and gases
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3
Q

What is the pathophysiology of disease for COPD?

A
  • Airway inflammation, airway fibrosis, and luminal plugs all cause increased airway resistance
  • Loss of alveolar attachments and decrease of elastic recoil lead to parenchymal destruction
  • Results in airflow limitation
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4
Q

What conditions make up COPD?

A
  • Chronic bronchitis (due inwards inflammation of small airways)
  • Emphysema
  • Asthma
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5
Q

What is the aetiology of COPD?

A
  • Biomass exposure
  • Smoking
  • Genetic (alpha 1 anti-trypsin deficiency)
  • Air pollution
  • Illicit drug use
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6
Q

What accelerates onset of COPD?

A
  • Not everybody’s lungs grow to full capacity
  • E.g. due to prematurity, poor nutrition, poor socio-economic background
  • Less lung capacity to lose accelerates onset of COPD
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7
Q

How is COPD diagnosed?

A
  • Symptoms e.g. SOB, chronic cough, sputum
  • Risk factors e.g. host factors, tobacco, occupation, pollution
  • Spirometry is required to establish diagnosis
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8
Q

What are the symptoms of COPD?

A
  • Dyspnoea
  • Chronic cough
  • Chronic sputum production
  • Recurrent lower respiratory tract infections
  • History of risk factors
  • Family history of COPD and/or childhood factors
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9
Q

What is dyspnoea like in COPD?

A
  • Progressive over time
  • Characteristically worse with exercise
  • Persistent
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10
Q

What is a chronic cough like in COPD?

A
  • May be intermittent and may be unproductive
  • Recurrent wheeze
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11
Q

What are the risk factors that may lead to COPD?

A
  • Host factors (genetic factors, congenital/developmental abnormalities etc.)
  • Tobacco smoke
  • Smoke from home cooking and heating fuels
  • Occupational dusts, vapours, fumes, gases and other chemicals
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12
Q

What childhood factors might predispose someone to COPD?

A
  • Low birthweight
  • Childhood respiratory infections
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13
Q

What are the signs of COPD?

A
  • Purse lip breathing
  • Hyperinflation or barrel-shaped chest
  • Prolonged expiratory phase
  • Maybe wheeze on auscultation
  • In advanced cases: cyanosis and cor pulmonale
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14
Q

Outline how spirometry works

A
  • Measure of how much and how fast a person can breathe out
  • Patient takes a deep breath and blows as hard as possible into tube
  • Technician monitors and encourages patient during test
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15
Q

What does spirometry measure?

A
  • Forced expiratory volume in 1 second
  • Full vital capacity i.e. how much air is expelled in one breath
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16
Q

How does COPD change spirometry traces?

A
  • Takes longer to breathe out due to obstruction
  • FVC and FEV1 are decreased
  • FVC:FEV1 ratio decreases
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17
Q

What other investigations are used to identify COPD?

A
  • Chest X-ray
  • HRCT
  • Full pulmonary function tests
  • ABG if suspicion of respiratory failure
  • Alpha-1- antitrypsin deficiency blood test for younger patients
18
Q

Why is a chest X-ray used in patients with COPD?

A
  • May suggest hyperinflation
  • Mandatory to exclude other diagnoses
19
Q

Why is HRCT used in patients with COPD?

A
  • Detailed assessment of degree of emphysema
  • If suspicion of bronchiectasis
  • Not required for routine assessment of COPD
20
Q

Why are full pulmonary function tests used in patients with COPD?

A
  • Static lung volumes can assess for hyperinflation
  • Gas transfer to look at alveolar destruction
21
Q

Define an exacerbation of COPD

A
  • An acute worsening of respiratory symptoms that result in additional therapy
22
Q

What common bacteria cause COPD exacerbations?

A
  • Haemophilus influenzae
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
23
Q

What common viral pathogens cause COPD exacerbations?

A
  • Rhinoviruses
  • Coronavirus
  • Influenza
24
Q

What therapies for COPD improve symptoms?

A
  • Pulmonary rehabilitation
  • Bronchodilators (beta 2 agonists and anti-muscarinics)
  • Mucolytics
    -Lung volume reduction surgery
  • Lung transplant
25
Q

What therapies improve risk in COPD?

A
  • Smoking cessation
  • Anti-inflammatories (inhaled corticosteroids and long-term macrolides)
  • Oxygen therapy
  • Non-invasive ventilation
26
Q

How does smoking cessation improve COPD?

A
  • Reduces mortality
  • Improves symptoms
  • Slows down loss of lung function
  • Reduces exacerbations
  • Drugs work better
27
Q

What therapies can help patients to stop smoking?

A
  • Nicotine replacement therapy
  • Champix
  • Behavioural support
  • Vaping
28
Q

What does pulmonary rehabilitation entail?

A
  • 6-8 week course
  • Hospital or community basis
  • 2 supervised sessions/week
  • 1 unsupervised/week
  • Education programme
  • Referral or ongoing plan onto maintenance therapy
29
Q

What are the effects of antimuscarinic agents on the airways?

A
  • More effective in proximal airways
  • Inhibit bronchoconstrictor effect of ACh at M3 muscarinic receptors located on airway smooth muscle
30
Q

What are the effects of B2 agonists?

A
  • More effective in distal airways
  • Directly activate B2 receptors in bronchioles, leading to increase in cAMP, relaxation of smooth muscle, and bronchodilation
31
Q

What are the effects of inhaled corticosteroids?

A
  • Reduce exacerbation frequency
32
Q

Outline long term oxygen therapy

A
  • Extended periods of hypoxaemia cause end-organ damage to heart and kidneys
  • Given if pO2 <7.3kPa at rest
  • For minimum 16 hours/day
  • Improves survival
  • Non-smokers
  • Safety - home fire risk assessment (O2 is very flammable)
33
Q

Outline ambulatory oxygen

A
  • If patients desaturate by >4% when walking
  • Use during exertion
  • Need to walk further on oxygen
  • No prognostic benefit
34
Q

What are the symptoms of bronchiectasis?

A
  • Cough with sputum - produce an eggcup of sputum per day
  • Breathlessness
  • Recurrent infections/exacerbations
  • Haemoptysis
  • Weight loss/fatigue/exercise limitation
35
Q

What are the causes of bronchiectasis?

A
  • Post-infectious (TB, pneumonia, whooping cough)
  • Immunodeficiency
  • Impaired muco-ciliary clearance
  • Airways lesions
  • Other chronic respiratory disorders (COPD)
  • Auto-immune
  • Other syndromes (Marfans, polycystic kidney disease)
36
Q

How is bronchiectasis diagnosed?

A
  • Productive cough
  • Crackles on auscultation
  • Hallmarks of other disease
  • CXR
  • CT scan
  • Bloods
37
Q

How is bronchiectasis treated?

A
  • Airways clearance (physiotherapy, active cycle technique, adjuvant inhaled therapy, mucolytics)
  • Low-dose macrolides (antibiotics with anti-inflammatory effect)
  • Inhaled corticosteroids and bronchodilators
38
Q

What additional infections can patients with bronchiectasis cause?

A
  • Pseudomonas aeruginosa
  • Non-tuberculous mycobacteria
39
Q

How does pseudomonas aeruginosa affect patients with bronchiectasis?

A
  • Patients become chronically colonised
  • Worsens disease and increases exacerbations
  • Limited antibiotics coverage (use ciprofloxacin)
  • Treatment involves eradication therapy, nebulised colomycin, easy access to IV abx)
40
Q

How does non-tuberculous mycobacteria (NTM) affect patients with bronchiectasis?

A
  • Need to screen for it
  • Often incidental finding and doesn’t usually need treating
  • Some are very aggressive
  • 18 month broad spectrum antibiotics
41
Q

What is bronchiectasis?

A
  • An uncommon condition resulting in dilated, damaged airways
  • Results in sputum build up and inflammation
42
Q

Outline the pathophysiology of cystic fibrosis

A
  • Defect on long arm of chromosome 7
  • Leads to CFTR mutation
  • Leads to ineffective cell surface chloride transport
  • Thick, dehydrated body fluid in organs which have CFTR

Respiratory (21 decks)

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