Phase 2 Kirsty McLauchlan and Vicky Cox
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Transcript of Phase 2 Kirsty McLauchlan and Vicky Cox
Phase 2
Kirsty McLauchlan and Vicky Cox
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• Asthma• COPD• Pulmonary Fibrosis
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Aims
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Introduction
• A chronic relapsing/episodic inflammatory condition of the airways
• Characterised by 1. Airflow limitation2. Airway hyper-responsiveness3. Bronchial inflammation
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Asthma
• 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 - Epidemiology
Asthma
Extrinsic Intrinsic
Childhood – atopic Middle-aged Late onset – occupational
- NSAID-intolerance- β-adrenoreceptor blocking agents
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Asthma – Aetiology (cause)Not
immunologically mediated
Type I hypersensitivity
reactions
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Asthma - triggersALLERGENS (atopy)
Viral infection
Cold air
Emotion
Irritant dusts, vapor, fumes(cigarette smoke)
Occupationalsensitizers
Atmospheric pollution
Exercise
Drugs – NSAIDs, β-adrenoreceptor blocking agents
• 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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Asthma – what is Atopy?
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Occupational Asthma
animals latex dyes
bleachWood dustAntibioticsFlour
paints
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Asthma - Pathogenesis
InflammationMucus and oedemaBronchoconstriction
AIRWAY OBSTRUCTION REMODELING
EpitheliumSmooth muscle
Basement membrane
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Asthma 1. INFLAMMATION
• IgE = bronchoconstriction• By blocking β-adrenoreceptor in smooth
muscle surrounding airways
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Asthma – 2. Bronchoconstriction
This is why β-adrenoreceptor blockers (e.g propranolol) can trigger asthmatic response!
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Asthma 3. oedema + mucus
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Asthma - remodeling• Hypertrophy• Contractility
• Loss of cilia• Goblet cells= more infection+ more mucus
Deposition of collagen = thickened basement membrane
• Episodes/attack of shortness of breath and wheezing
• Bilateral, polyphonic, expiratory, widespread• Worse at night• Cough
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Asthma – Clinical Features
• Spirometry – reduced FEV1 • PEF – reduced
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Asthma – investigations
• 15% improvement in either after a bronchodilator indicates asthma
• Exercise tests• Blood count – eosinophils• Exhaled nitric oxide - eosinophils
• Controlling extrinsic factors
• Long term treatment
• Treatment of acute attack
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Asthma - Treatment
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Asthma - Pathogenesis
InflammationMucus and oedemaBronchoconstriction
AIRWAY OBSTRUCTION REMODELING
EpitheliumSmooth muscle
Basement membraneB2-agonistB2-agonist
corticosteroidcorticosteroid
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Step-wise management
salbutamol
budesonide
salmeterol
monteleukast
prednisolone
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Management of Acute Attack
IV aminophylline
Practice Questions
• ‘A common progressive disorder characterized by airway obstruction with little or no reversibility’
– Chronic bronchitis– Empyhsema
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Chronic Obstructive Pulmonary Disease
Obstructive:
- FEV1 (<80% predicted)- FEV1/FVC (<0.7 predicted)
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COPD
•Prevalence: 10-20% of over-40s
•2.5 x 106 deaths worldwide
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COPD - epidemiology
•caused by long-term exposure to toxic particles
– (cigarette smoking >90% of cases)
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COPD - aetiology
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COPD - pathophysiology
Neutrophils & CD8 lymphocytes
Inactivation of α1-antitrypsin by cigarette smoke
Columnar cells are replaced by squamous cells
Widespread narrowing of small ariways
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COPD - pathophysiology
Early disease, predominantly in the small airways, is reversible.
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COPD - pathophysiology
With mucous gland hypertrophy
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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
• loss of alveolar walls reduced elastic recoil• loss of alveolar supporting structure
Reduced surface for gas exchange
Airflow limitation
• “cough and sputum production on most days for 3 months of 2 successive years”
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Chronic Bronchitis
• “ enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls”
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Emphysema
• Productive cough •White or clear sputum•Wheeze•Dyspnoea
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Symptoms of COPD
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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COPD vs. Asthma
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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Signs of COPD
Normally respiratory drive is largely initiated by PaCO2.
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Pink Puffers/Blue Bloaters
-PaO2 < 8kPa
-PaCO2 > 7kPa
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Respiratory Failure
“heart disease secondary to respiratory disease”
•Pulmonary hypertension•Right ventricular hypertrophy•Right heart failure
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Cor Pulmonale
• Dyspnoea• Fatigue• Syncope• Cyanosis• Tachycardia• Raised JVP• RV Heave • Loud P2
•Pansystolic Murmur– tricuspic regurgitation
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Cor Pulmonale – clinical features
• Lung Function tests (↓FEV1:FVC, ↓ PEFR)
• Chest X-ray (often normal)
• High-resolution CT (to show bullae in empyhsema)
• Blood gases (often normal)The Peer Teaching Society is not liable for false or misleading information…
COPD - Investigations
• 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 – Assessing Severity
• 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
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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 - Treatment
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COPD – Acute Management
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COPD – Acute Management
• 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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Pulmonary Fibrosis – (interstitial lung disease)
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Acute and Chronic
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ACEPT A - Ankylosing spondylitisC – CancerE – Extrinsic allergic alveolitisP – PneumoconiosisT - 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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123
1 – primary pulmonary fibrosis2 – secondary pulmonary fibrosis
3 - asbestosis
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DiffuseChemotherapy
DrugsRadiation
And progression of disease
• Scarred lungs • Breathlessness• Dry cough• Fatigue• Clubbing
• RESTRICTIVE
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Clinical Picture
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• Remove offending agent• Suppress inflammation (glucocorticosteroids)• Manage hypoxemia
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Treatment depends on cause
Practice Questions