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Phase 2
Kirsty McLauchlan and Vicky Cox
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Aims
• Asthma
• COPD
• Pulmonary Fibrosis
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Introduction
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Asthma
• A chronic relapsing/episodic inflammatory
condition of the airways
• Characterised by
1.
2.
3.
Airflow limitation
Airway hyper-responsiveness
Bronchial inflammation
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Asthma - Epidemiology
• 15 % of population
• 5.2 million people in UK – 1.1million children
• Prevalence is increasing
• More in developed counties eg. UK, NZ, Australia
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Asthma – Aetiology (cause)
Type I
hypersensitivity
reactions
Asthma
Extrinsic
Childhood – atopic
Late onset – occupational
- NSAID-intolerance
- β-adrenoreceptor blocking agents
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Not
immunologically
mediated
Intrinsic
Middle-aged
Asthma - triggers
ALLERGENS (atopy)
Occupational
sensitizers
Atmospheric pollution
Exercise
Drugs – NSAIDs,
β-adrenoreceptor blocking agents
Viral infection
Cold air
Emotion
Irritant dusts, vapor, fumes
(cigarette smoke)
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Asthma – what is Atopy?
• Type of hypersensitivity – (Type 1)
• Runs in families
• Have increased IgE antibodies – allergen
specific
• Can be caused by environmental factors
– Early exposure to allergens
– Maternal smoking
– Hygiene hypothesis
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Occupational Asthma
animals
latex
paints
Antibiotics
Flour
dyes
Wood dust
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bleach
Asthma - Pathogenesis
AIRWAY
OBSTRUCTION
Inflammation
Mucus and oedema
Bronchoconstriction
REMODELING
Epithelium
Smooth muscle
Basement membrane
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Asthma 1. INFLAMMATION
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Asthma – 2. Bronchoconstriction
• IgE = bronchoconstriction
• By blocking β-adrenoreceptor in smooth
muscle surrounding airways
This is why β-adrenoreceptor blockers (e.g propranolol) can trigger asthmatic response!
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Asthma 3. oedema + mucus
Smooth
muscle
contraction
Histamine
Vascular
permeability
(oedema)
Bronchial
secretions
(mucus plug)
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Asthma - remodeling
• Hypertrophy
• Contractility
Smooth
muscle
Epithelium
Basement
membrane
Deposition of collagen =
thickened basement membrane
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• Loss of cilia
• Goblet cells
= more infection
+ more mucus
Asthma – Clinical Features
• Episodes/attack of shortness of breath and
wheezing
• Bilateral, polyphonic, expiratory, widespread
• Worse at night
• Cough
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Asthma – investigations
• Spirometry – reduced FEV1
• PEF – reduced
• 15% improvement in either after a
bronchodilator indicates asthma
• Exercise tests
• Blood count – eosinophils
• Exhaled nitric oxide - eosinophils
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Asthma - Treatment
• Controlling extrinsic factors
• Long term treatment
• Treatment of acute attack
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Asthma - Pathogenesis
AIRWAY
OBSTRUCTION
corticosteroid
B2-agonist
Inflammation
Mucus and oedema
Bronchoconstriction
REMODELING
Epithelium
Smooth muscle
Basement membrane
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Step-wise management
Occasional symptoms • Avoid extrinsic factors salbutamol
• Short acting B2agonists– ‘2 puffs as required’
PEFR 100%
Symptoms >3 a week
PEFR <80%
Severe symptoms
PEFR 50-80%
Continue severe symptoms
PEFR 50-80%
Severe deteriorating symptoms
PEFR <50%
Severe deteriorating symptoms
• Low dose inhaled corticosteroid
budesonide
salmeterol
• Add long acting B2-agonist
• High dose corticosteroid
monteleukast
• Consider leukotriene receptor antagonist
prednisolone
• Add oral corticosteroids daily
• Hospital admission
PEFRThe<30%
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Management of Acute Attack
Moderate
Severe
Life
Threatening
Able to talk
Not complete sentences
Resp < 25
Resp > 25
Silent chest
Pulse <110
Pulse > 110
Cyanosis
Sats > 92
Sats >92
Hypotension, bradycardia
PEF > 50%
PEF 33-50%
Sats < 92
Short acting B2 agonist
High flow oxygen
Oxygen + SABA +
corticosteroid +
antimuscarinic
+
+ SABA and corticosterois
Corticosteroid
+
antimuscarinic
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IV aminophylline
Practice Questions
Chronic Obstructive Pulmonary Disease
• ‘A common progressive disorder characterized
by airway obstruction with little or no
reversibility’
– Chronic bronchitis
– Empyhsema
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COPD
Obstructive:
- FEV1
(<80% predicted)
- FEV /FVC (<0.7 predicted)
1
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COPD - epidemiology
•Prevalence: 10-20% of over-40s
•2.5 x 106 deaths worldwide
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COPD - aetiology
•caused by long-term exposure to toxic particles
– (cigarette smoking >90% of cases)
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COPD - pathophysiology
Inactivation of α1antitrypsin by
cigarette smoke
Infiltration of the
bronchi/bronchiole
walls with
inflammatory cells
Neutrophils & CD8
lymphocytes
Widespread
narrowing of small
ariways
Granulocytes
release elasteases
and proteases
Ulceration, scarring
& columnar cell
metaplasia
Columnar cells are
replaced by
squamous cells
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COPD - pathophysiology
Early disease, predominantly in the small
airways, is reversible.
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COPD - pathophysiology
Progressive
squamous cell
metaplasia
Fibrosis of bronchial
walls
With mucous gland
hypertrophy
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Airflow
limitation/narrowing
Chronic Bronchitis - pathophysiology
• Lumen occlusion by mucus plugging
• Goblet cell metaplasia
.
• Smooth muscle hyperplasia
• Distortion due to fibrosis
Airway
narrowing
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Emphysema - pathophysiology
• permanent enlargement of airspaces
Reduced surface
.
for gas exchange
• loss of alveolar walls  reduced elastic recoil
• loss of alveolar supporting structure
Airflow limitation
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Chronic Bronchitis
• “cough and sputum production on most days
for 3 months of 2 successive years”
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Emphysema
• “ enlarged air spaces distal to terminal
bronchioles, with destruction of alveolar
walls”
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Symptoms of COPD
• Productive cough
•White or clear sputum
•Wheeze
•Dyspnoea
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COPD vs. Asthma
COPD:
- age of onset > 35 years
- smoking (active or passive)
- chronic dyspnoea
- sputum production
- minimal diurnal or day-to-day FEV1 variation
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Signs of COPD
Mild disease: no signs or quiet wheeze
Severe disease: - tachypnoea
- prolonged expiration
- use of accessory muscles
- intercostal indrawing
- lip-pursed expiration
- poor chest expansion
- hyperinflated lungs
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Signs of COPD
Mild disease: no signs or quiet wheeze
Severe disease: - tachypnoea
- prolonged expiration
- use of accessory muscles
- intercostal indrawing
- lip-pursed expiration
- poor chest expansion
- hyperinflated lungs
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Pink Puffers/Blue Bloaters
Normally respiratory drive is largely initiated by PaCO2.
Pink Puffers
• ↑ alveolar ventilation
• Normal PaO2, normal or low
PaCO2
• breathless, not cyanosed
• may  Type 1 Resp. Failure
Blue Bloaters
•
•
•
•
•
↓ alveolar ventilation
Low PaO2, high PaCO2
cyanosed, not breathless
May  cor pulmonale
HYPOXIC DRIVE
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Respiratory Failure
-PaO2 < 8kPa
-PaCO2 > 7kPa
Chronic alveolar
hypoxia +
hypercapnia
Constriction of
pulmonary
arterioles
Pulmonary
arterial
hypertension
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Cor Pulmonale
“heart disease secondary to respiratory disease”
•Pulmonary hypertension
•Right ventricular hypertrophy
•Right heart failure
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Cor Pulmonale – clinical features
• Dyspnoea
• Fatigue
• Syncope
• Cyanosis
• Tachycardia
• Raised JVP
• RV Heave
• Loud P2
•Pansystolic Murmur
– tricuspic regurgitation
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COPD - Investigations
• Lung Function tests (↓FEV1:FVC, ↓ PEFR)
• Chest X-ray (often normal)
• High-resolution CT (to show bullae in
empyhsema)
• Blood gases (often normal)
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COPD – Assessing Severity
• British Thoracic Society/NICE COPD guidelines
– Mild: FEV1 50-80% of predicted
– Moderate: FEV1 30-49% of predicted
–Severe: FEV1 <30% of predicted
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COPD – Treatment
• General Treatments
– stop smoking
– encourage exercise
– treat poor nutrition or obesity
– influenza and pneumococcal vaccinations
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COPD - Treatment
Initial Treatment
Antimuscarinic (e.g. Ipratropium) or β2 agonist
(e.g. Salbutamol) inhaled PRN
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COPD - Treatment
Persistent
breathlessness or
exacerbations
FEV1 > 50%
LABA
(Long-acting Beta2
Agonist)
FEV1 < 50%
LAMA
(Long-acting
Muscarinic
Antagonist)
LABA + ICS
(combined
inhaler)
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LAMA
COPD - Treatment
Severe Disease
LABA + Inhaled Steroid + Anticholinergic
+ Refer to specialist
+ Consider steroid trial
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COPD - Treatment
Long Term Oxygen Therapy
Consider LTOT if PaO2 <7.3kPa
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COPD – Acute Management
• Controlled Oxygen Therapy
• Start at 24-28%
• Aim for PaO2 > 8.0kPa
• Nebulised Bronchodilators
• Salbutamol 5mg/4h + Ipratropium 500ug/6h
• Steroids
• IV Hydrocortisone 200mg + Oral Prednisalone 30-40mg
(continue for 10-14 days)
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COPD – Acute Management
• Antibiotics
• Use if evidence of infection
• e.g. Amoxicillin 500mg/8h PO
• Physiotherapy
• To aid sputum expectoration
• If not response, consider
• Repeat Nebs, consider IV aminophylline, NIPPV etc.
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Pulmonary Fibrosis – (interstitial lung disease)
• Also known as diffuse parenchymal lung
disorders
• Collection of disorders affecting
– Alveoli
– Alveolar epithelium
– Capillary endothelium
– And the spaces in-between
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Acute and Chronic
Interstitial Lung Disease
Acute
Chronic
Hypersensitivity pneumonitis
Adult respiratory distress syndrome
Drug/toxin reaction
Interstitial pneumonia = idiopathic
pulmonary fibrosis
Radiation pneumonitis
Sarcoidosis
Trauma
Pneumoconiosis (occupational)
Infection
Rheumatoid / SLE
Asbestos
Diffuse malignancy
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ACEPT
A - Ankylosing spondylitis
C – Cancer
E – Extrinsic allergic alveolitis
P – Pneumoconiosis
T - TB
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SARCOIDOSIS
•
•
•
•
•
Multisystem granulomatous disorder
Affects age 30-40
Pulmonary infiltration
Often no symptoms
If persists over 6 months treat with prednisolone
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1 – primary pulmonary fibrosis
2 – secondary pulmonary fibrosis
3 - asbestosis
1
2
3
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Diffuse
Chemotherapy
Drugs
Radiation
And progression of disease
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Clinical Picture
•
•
•
•
•
Scarred lungs
Breathlessness
Dry cough
Fatigue
Clubbing
• RESTRICTIVE
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Obstructive
•Hard to exhale
FEV1 TLC
• Asthma, COPD,
bronchiectasis, cystic
fibrosis
Restrictive
• Difficult to
expand lungs
FVC
• Pulmonary fibrosis,
obesity, neuromuscular,
sarcoidosis
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Treatment depends on
cause
• Remove offending agent
• Suppress inflammation (glucocorticosteroids)
• Manage hypoxemia
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Practice Questions