Phase 2 Kirsty McLauchlan and Vicky Cox The Peer Teaching Society is not liable for false or misleading information…

Phase 2

Kirsty McLauchlan and Vicky Cox

The Peer Teaching Society is not liable for false or misleading information…

• Asthma• COPD• Pulmonary Fibrosis

Introduction

• A chronic relapsing/episodic inflammatory condition of the airways

• Characterised by 1. Airflow limitation2. Airway hyper-responsiveness3. Bronchial inflammation

Asthma

• 15 % of population• 5.2 million people in UK – 1.1million children

• Prevalence is increasing

• More in developed counties eg. UK, NZ, Australia

Asthma - Epidemiology

Asthma

Extrinsic Intrinsic

Childhood – atopic Middle-aged Late onset – occupational

- NSAID-intolerance- β-adrenoreceptor blocking agents

Asthma – Aetiology (cause)Not

immunologically mediated

Type I hypersensitivity

reactions

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

Asthma – what is Atopy?

Occupational Asthma

animals latex dyes

bleachWood dustAntibioticsFlour

paints

Asthma - Pathogenesis

InflammationMucus and oedemaBronchoconstriction

AIRWAY OBSTRUCTION REMODELING

EpitheliumSmooth muscle

Basement membrane

Asthma 1. INFLAMMATION

• IgE = bronchoconstriction• By blocking β-adrenoreceptor in smooth

muscle surrounding airways

Asthma – 2. Bronchoconstriction

This is why β-adrenoreceptor blockers (e.g propranolol) can trigger asthmatic response!

Asthma 3. oedema + mucus

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

Asthma – Clinical Features

• Spirometry – reduced FEV1 • PEF – reduced

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

Asthma - Treatment

Asthma - Pathogenesis

InflammationMucus and oedemaBronchoconstriction

AIRWAY OBSTRUCTION REMODELING

EpitheliumSmooth muscle

Basement membraneB2-agonistB2-agonist

corticosteroidcorticosteroid

Step-wise management

salbutamol

budesonide

salmeterol

monteleukast

prednisolone

Management of Acute Attack

IV aminophylline

Practice Questions

• ‘A common progressive disorder characterized by airway obstruction with little or no reversibility’

– Chronic bronchitis– Empyhsema

Chronic Obstructive Pulmonary Disease

Obstructive:

- FEV1 (<80% predicted)- FEV1/FVC (<0.7 predicted)

•Prevalence: 10-20% of over-40s

•2.5 x 106 deaths worldwide

COPD - epidemiology

•caused by long-term exposure to toxic particles

– (cigarette smoking >90% of cases)

COPD - aetiology

COPD - pathophysiology

Neutrophils & CD8 lymphocytes

Inactivation of α1-antitrypsin by cigarette smoke

Columnar cells are replaced by squamous cells

Widespread narrowing of small ariways

Early disease, predominantly in the small airways, is reversible.

With mucous gland hypertrophy

Chronic Bronchitis - pathophysiology

• Lumen occlusion by mucus plugging• Goblet cell metaplasia• Smooth muscle hyperplasia• Distortion due to fibrosis

Airway narrowing

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”

Chronic Bronchitis

• “ enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls”

Emphysema

• Productive cough •White or clear sputum•Wheeze•Dyspnoea

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

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

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

Signs of COPD

Normally respiratory drive is largely initiated by PaCO2.

Pink Puffers/Blue Bloaters

-PaO2 < 8kPa

-PaCO2 > 7kPa

Respiratory Failure

“heart disease secondary to respiratory disease”

•Pulmonary hypertension•Right ventricular hypertrophy•Right heart failure

Cor Pulmonale

• Dyspnoea• Fatigue• Syncope• Cyanosis• Tachycardia• Raised JVP• RV Heave • Loud P2

•Pansystolic Murmur– tricuspic regurgitation

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

COPD – Assessing Severity

• General Treatments– stop smoking– encourage exercise– treat poor nutrition or obesity– influenza and pneumococcal vaccinations

COPD – Treatment

Initial Treatment

Antimuscarinic (e.g. Ipratropium) or β2 agonist (e.g. Salbutamol) inhaled PRN

COPD - Treatment

Severe Disease

LABA + Inhaled Steroid + Anticholinergic

+ Refer to specialist

+ Consider steroid trial

COPD - Treatment

Long Term Oxygen Therapy

Consider LTOT if PaO2 <7.3kPa

COPD - Treatment

COPD – Acute Management

• Also known as diffuse parenchymal lung disorders

• Collection of disorders affecting – Alveoli– Alveolar epithelium– Capillary endothelium– And the spaces in-between

Pulmonary Fibrosis – (interstitial lung disease)

Acute and Chronic

ACEPT A - Ankylosing spondylitisC – CancerE – Extrinsic allergic alveolitisP – PneumoconiosisT - TB

SARCOIDOSIS

• Multisystem granulomatous disorder• Affects age 30-40• Pulmonary infiltration• Often no symptoms• If persists over 6 months treat with prednisolone

1 – primary pulmonary fibrosis2 – secondary pulmonary fibrosis

3 - asbestosis

DiffuseChemotherapy

DrugsRadiation

And progression of disease

• Scarred lungs • Breathlessness• Dry cough• Fatigue• Clubbing

• RESTRICTIVE

Clinical Picture

• Remove offending agent• Suppress inflammation (glucocorticosteroids)• Manage hypoxemia

Treatment depends on cause

Practice Questions

Phase 2 Kirsty McLauchlan and Vicky Cox The Peer Teaching Society is not liable for false or misleading information…

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