phase 2 kirsty mclauchlan and vicky cox
DESCRIPTION
Respiratory. Phase 2 Kirsty McLauchlan and Vicky Cox. The Peer Teaching Society is not liable for false or misleading information…. Aims. Asthma COPD Pulmonary Fibrosis. The Peer Teaching Society is not liable for false or misleading information…. Introduction. - PowerPoint PPT PresentationTRANSCRIPT
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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
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• A chronic relapsing/episodic inflammatory condition of the airways
• Characterised by 1. Airflow limitation2. Airway hyper-responsiveness3. Bronchial inflammation
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Asthma
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• 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
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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
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• 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
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• 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
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• Episodes/attack of shortness of breath and wheezing
• Bilateral, polyphonic, expiratory, widespread• Worse at night• Cough
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Asthma – Clinical Features
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• 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
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• 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
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Practice Questions
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• ‘A common progressive disorder characterized by airway obstruction with little or no reversibility’
– Chronic bronchitis– Empyhsema
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Chronic Obstructive Pulmonary Disease
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Obstructive:
- FEV1 (<80% predicted)- FEV1/FVC (<0.7 predicted)
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COPD
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•Prevalence: 10-20% of over-40s
•2.5 x 106 deaths worldwide
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COPD - epidemiology
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•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
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• “cough and sputum production on most days for 3 months of 2 successive years”
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Chronic Bronchitis
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• “ enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls”
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Emphysema
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• Productive cough •White or clear sputum•Wheeze•Dyspnoea
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Symptoms of COPD
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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
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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
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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
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Normally respiratory drive is largely initiated by PaCO2.
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Pink Puffers/Blue Bloaters
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-PaO2 < 8kPa
-PaCO2 > 7kPa
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Respiratory Failure
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“heart disease secondary to respiratory disease”
•Pulmonary hypertension•Right ventricular hypertrophy•Right heart failure
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Cor Pulmonale
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• Dyspnoea• Fatigue• Syncope• Cyanosis• Tachycardia• Raised JVP• RV Heave • Loud P2
•Pansystolic Murmur– tricuspic regurgitation
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Cor Pulmonale – clinical features
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• 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
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• 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
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• General Treatments– stop smoking– encourage exercise– treat poor nutrition or obesity– influenza and pneumococcal vaccinations
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COPD – Treatment
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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
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Severe Disease
LABA + Inhaled Steroid + Anticholinergic
+ Refer to specialist
+ Consider steroid trial
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COPD - Treatment
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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
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• 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
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• 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
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Practice Questions